Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride.

PubMed

Panneerselvam, Lakshmikanthan; Raghunath, Azhwar; Perumal, Ekambaram

2017-09-01

Acute fluoride (F - ) toxicity is known to cause severe cardiac complications and leads to sudden heart failure. Previously, we reported that increased myocardial oxidative damage, apoptosis, altered cytoskeleton and AMPK signaling proteins associated with energy deprivation in acute F - induced cardiac dysfunction. The present study was aimed to decipher the status of myocardial heat shock proteins (Hsps-Hsp27, Hsp32, Hsp40, Hsp60, Hsp70, Hsp90) and heat shock transcription factor 1 (Hsf1) in acute F - -intoxicated rats. In order to study the expression of myocardial Hsps, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F - for 24 h. The expression levels of myocardial Hsps were determined using RT-PCR, western blotting, and immunohistochemical studies. Acute F - -intoxicated rats showed elevated levels of both the transcripts and protein expression of Hsf1, Hsp27, Hsp32, Hsp60, and Hsp70 when compared to control. In addition, the expression levels of Hsp40 and Hsp90 were significantly declined in a dose-dependent fashion in F - -treated animals. Our result suggests that differential expression of Hsps in the rat myocardium could serve as a balance between pro-survival and death signal during acute F - -induced heart failure.

Rationale and Design of a Clinical Trial to Evaluate the Safety and Efficacy of Intracoronary Infusion of Allogeneic Human Cardiac Stem Cells in Patients With Acute Myocardial Infarction and Left Ventricular Dysfunction: The Randomized Multicenter Double-Blind Controlled CAREMI Trial (Cardiac Stem Cells in Patients With Acute Myocardial Infarction).

PubMed

Sanz-Ruiz, Ricardo; Casado Plasencia, Ana; Borlado, Luis R; Fernández-Santos, María Eugenia; Al-Daccak, Reem; Claus, Piet; Palacios, Itziar; Sádaba, Rafael; Charron, Dominique; Bogaert, Jan; Mulet, Miguel; Yotti, Raquel; Gilaberte, Immaculada; Bernad, Antonio; Bermejo, Javier; Janssens, Stefan; Fernández-Avilés, Franciso

2017-06-23

Stem cell therapy has increased the therapeutic armamentarium in the fight against ischemic heart disease and heart failure. The administration of exogenous stem cells has been investigated in patients suffering an acute myocardial infarction, with the final aim of salvaging jeopardized myocardium and preventing left ventricular adverse remodeling and functional deterioration. However, phase I and II clinical trials with autologous and first-generation stem cells have yielded inconsistent benefits and mixed results. In the search for new and more efficient cellular regenerative products, interesting cardioprotective, immunoregulatory, and cardioregenerative properties have been demonstrated for human cardiac stem cells. On the other hand, allogeneic cells show several advantages over autologous sources: they can be produced in large quantities, easily administered off-the-shelf early after an acute myocardial infarction, comply with stringent criteria for product homogeneity, potency, and quality control, and may exhibit a distinctive immunologic behavior. With a promising preclinical background, CAREMI (Cardiac Stem Cells in Patients With Acute Myocardial Infarction) has been designed as a double-blind, 2:1 randomized, controlled, and multicenter clinical trial that will evaluate the safety, feasibility, and efficacy of intracoronary delivery of allogeneic human cardiac stem cell in 55 patients with large acute myocardial infarction, left ventricular dysfunction, and at high risk of developing heart failure. This phase I/II clinical trial represents a novel experience in humans with allogeneic cardiac stem cell in a rigorously imaging-based selected group of acute myocardial infarction patients, with detailed safety immunologic assessments and magnetic resonance imaging-based efficacy end points. URL: http://www.clinicaltrials.gov. Unique identifier: NCT02439398. © 2017 American Heart Association, Inc.

3D cardiac wall thickening assessment for acute myocardial infarction

NASA Astrophysics Data System (ADS)

Khalid, A.; Chan, B. T.; Lim, E.; Liew, Y. M.

2017-06-01

Acute myocardial infarction (AMI) is the most severe form of coronary artery disease leading to localized myocardial injury and therefore irregularities in the cardiac wall contractility. Studies have found very limited differences in global indices (such as ejection fraction, myocardial mass and volume) between healthy subjects and AMI patients, and therefore suggested regional assessment. Regional index, specifically cardiac wall thickness (WT) and thickening is closely related to cardiac function and could reveal regional abnormality due to AMI. In this study, we developed a 3D wall thickening assessment method to identify regional wall contractility dysfunction due to localized myocardial injury from infarction. Wall thickness and thickening were assessed from 3D personalized cardiac models reconstructed from cine MRI images by fitting inscribed sphere between endocardial and epicardial wall. The thickening analysis was performed in 5 patients and 3 healthy subjects and the results were compared against the gold standard 2D late-gadolinium-enhanced (LGE) images for infarct localization. The notable finding of this study is the highly accurate estimation and visual representation of the infarct size and location in 3D. This study provides clinicians with an intuitive way to visually and qualitatively assess regional cardiac wall dysfunction due to infarction in AMI patients.

Sgarbossa criteria and acute myocardial infarction.

PubMed

Alang, Neha; Bathina, Jaya; Kranis, Mark; Angelis, Dimitrios

2010-01-01

Diagnosis of acute ST-elevation myocardial infarction in the presence of left bundle branch block is difficult. present a case of acute myocardial infarction with LBBB diagnosed and treated using the Sgarbossa criteria.

Myocardial oedema as the sole marker of acute injury in Takotsubo cardiomyopathy: a cardiovascular magnetic resonance (CMR) study.

PubMed

Iacucci, Ilaria; Carbone, Iacopo; Cannavale, Giuseppe; Conti, Bettina; Iampieri, Ilaria; Rosati, Riccardo; Sardella, Gennaro; Frustaci, Andrea; Fedele, Francesco; Catalano, Carlo; Francone, Marco

2013-12-01

The main hallmark of Takotsubo cardiomyopathy (TT-CMP) is transient ischaemia, with completely reversible regional contractile dysfunction, which involves the mid-apical segments and shows no angiographic signs of coronary artery disease (CAD). The acute and reversible myocardial injury suggests that tissue oedema may be an important marker of disease. Seventeen patients with a clinical and angiographic diagnosis of TT-CMP underwent cardiovascular magnetic resonance (CMR) imaging in the acute phase and at follow-up after 4 months. A standard acquisition protocol including turbo spin echo (TSE) T2-weighted short-tau inversion-recovery (T2 STIR), steady-state free-precession cine (SSFP cine) and lateenhancement (LE) imaging after gadolinium benzyloxypropionic tetraacetic acid (Gd-BOPTA) administration was performed. All images were analysed, and data on oedema and LE were correlated with regional dysfunction and histological findings from endomyocardial biopsy (EMB) where available. In all patients, T2 STIR images showed a diffuse homogeneous hyperintensity that extended to all mid-apical segments and perfectly matched the area of regional dysfunction, reflecting tissue oedema. In the five patients who underwent EMB, histology confirmed the massive interstitial oedema associated with typical contraction-band necrosis. No cases of LE were observed. At follow-up, complete regression of oedema was observed in all cases, with significant recovery of regional and global left ventricular (LV) function (ejection fraction from 48.7% to 59.8%). Myocardial oedema on CMR is a characteristic feature of acute TT-CMP, which reflects acute inflammation and acute myocardial injury. It could therefore be used as a specific marker of disease severity.

Relation of Erectile Dysfunction to Subclinical Myocardial Injury.

PubMed

Omland, Torbjørn; Randby, Anna; Hrubos-Strøm, Harald; Røsjø, Helge; Einvik, Gunnar

2016-12-15

The circulating concentration of cardiac troponin I (cTnI) is an index of subclinical myocardial injury in several patient populations and in the general population. Erectile dysfunction is associated with greater risk for cardiovascular events, but the association with subclinical myocardial injury is not known. We aimed to test the hypothesis that the presence and severity of erectile dysfunction is associated with greater concentrations of cTnI in the general population. The presence and severity of erectile dysfunction was assessed by administering the International Index of Erectile Function 5 (IIEF-5) questionnaire to 260 men aged 30 to 65 years recruited from a population-based study. Concentrations of cTnI were determined by a high-sensitivity (hs) assay. Hs-cTnI levels were significantly higher in subjects with than in those without erectile dysfunction (median 2.9 vs 1.6 ng/l; p <0.001). Men with erectile dysfunction (i.e., IIEF-5 sum score <22) were also significantly older; had a higher systolic blood pressure, lower estimated glomerular filtration rate, higher augmentation index and N-terminal pro-B-type natriuretic peptide; and had a higher prevalence of hypertension, diabetes mellitus, and previous coronary artery disease than subjects without erectile dysfunction. These covariates were adjusted for in a multivariate linear regression model, yet the IIEF-5 sum score remained significantly negatively associated with the hs-cTnI concentration (standardized β -0.206; p <0.001). In conclusion, the presence and severity of erectile dysfunction is associated with circulating concentrations of hs-cTnI, indicating subclinical myocardial injury independently of cardiovascular risk factors, endothelial dysfunction and heart failure biomarkers. Copyright © 2016 Elsevier Inc. All rights reserved.

Acute myocardial infarction with changing axis deviation.

PubMed

Patanè, Salvatore; Marte, Filippo

2011-07-01

Changing axis deviation has been rarely reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been rarely reported also during acute myocardial infarction associated with atrial fibrillation. Isolated left posterior hemiblock is a very rare finding but the evidence of transient right axis deviation with a left posterior hemiblock pattern has been reported during acute anterior myocardial infarction as related with significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery. Left anterior hemiblock development during acute inferior myocardial infarction can be an indicator of left anterior descending coronary artery lesions, multivessel coronary artery disease, and impaired left ventricular systolic function. We present a case of changing axis deviation in a 62-year-old Italian man with acute myocardial infarction. Also this case focuses attention on changing axis deviation during acute myocardial infarction. Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.

Calcineurin Regulates Myocardial Function during Acute Endotoxemia

PubMed Central

Joshi, Mandar S.; Julian, Mark W.; Huff, Jennifer E.; Bauer, John A.; Xia, Yong; Crouser, Elliott D.

2006-01-01

Rationale: Cyclosporin A (CsA) is known to preserve cardiac contractile function during endotoxemia, but the mechanism is unclear. Increased nitric oxide (NO) production and altered mitochondrial function are implicated as mechanisms contributing to sepsis-induced cardiac dysfunction, and CsA has the capacity to reduce NO production and inhibit mitochondrial dysfunction relating to the mitochondrial permeability transition (MPT). Objectives: We hypothesized that CsA would protect against endotoxin-mediated cardiac contractile dysfunction by attenuating NO production and preserving mitochondrial function. Methods: Left ventricular function was measured continuously over 4 h in cats assigned as follows: control animals (n = 7); LPS alone (3 mg/kg, n = 8); and CsA (6 mg/kg, n = 7), a calcineurin inhibitor that blocks the MPT, or tacrolimus (FK506, 0.1 mg/kg, n = 7), a calcineurin inhibitor lacking MPT activity, followed in 30 min by LPS. Myocardial tissue was then analyzed for NO synthase-2 expression, tissue nitration, protein carbonylation, and mitochondrial morphology and function. Measurements and Main Results: LPS treatment resulted in impaired left ventricular contractility, altered mitochondrial morphology and function, and increased protein nitration. As hypothesized, CsA pretreatment normalized cardiac performance and mitochondrial respiration and reduced myocardial protein nitration. Unexpectedly, FK506 pretreatment had similar effects, normalizing both cardiac and mitochondrial parameters. However, CsA and FK506 pretreatments markedly increased protein carbonylation in the myocardium despite elevated manganese superoxide dismutase activity during endotoxemia. Conclusions: Our data indicate that calcineurin is a critical regulator of mitochondrial respiration, tissue nitration, protein carbonylation, and contractile function in the heart during acute endotoxemia. PMID:16424445

Transient ventricular dysfunction after an asphyxiation event: stress or hypoxia?

PubMed

Valletta, Mary E; Haque, Ikram; Al-Mousily, Faris; Udassi, Jai; Saidi, Arwa

2008-11-01

This report of a pediatric patient with acute upper airway obstruction causing asphyxiation emphasizes the need to maintain clinical suspicion for acquired myocardial dysfunction, despite the presumed role of noncardiogenic causes for pulmonary edema after an acute upper airway obstruction. Case report. A tertiary pediatric intensive care unit. A 10-year-old girl with no significant medical history who developed flash pulmonary edema and acute myocardial dysfunction after an acute upper airway obstruction. Serial echocardiograms, exercise stress test, and coronary angiography were performed. Serial pro-brain natriuretic peptide, troponins, and CK-MB levels were also followed. Troponin level normalized approximately 7 days after the acute event. CK-MB and pro-brain natriuretic peptide levels decreased but had not completely normalized by time of discharge. The patient was discharged home 10 days after the event on an anticipated 6-month course of metoprolol without any signs or symptoms of cardiac dysfunction. Myocardial dysfunction is rarely documented in children after an acute upper airway obstruction or an asphyxiation event. Pediatric intensivists and hospitalists should maintain a high degree of clinical suspicion and screen for possible myocardial dysfunction in the pediatric patient with an acute severe hypoxic event especially when accompanied by pulmonary edema. Prompt evaluation ensures appropriate support. Additionally, some role may exist for early adrenergic receptor blockade.

Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury.

PubMed

McDonough, Kathleen H; Virag, Jitka Ismail

2006-01-01

Sepsis, bacteremia and inflammation cause myocardial depression. The mechanism of the dysfunction is not clearly established partly because dysfunction can be elicited by many different mechanisms which can all manifest in disruption of myocardial mechanical function. In addition the models of sepsis and bacteremia and inflammation may vary drastically in the sequence of the coordinated immune response to the inflammatory or septic stimulus. Patterns of cytokine expression can vary as can other responses of the immune system. Patterns of neurohumoral activation in response to the stress of sepsis or bacteremia or inflammation can also vary in both magnitude of response and temporal sequence of response. Stress induced activation of the sympathetic nervous system and humoral responses to stress have a wide range of intensity that can be elicited. The fairly uniform response of the myocardium indicating cardiac dysfunction is surprisingly constant. Systolic performance, as measured by stroke volume or cardiac output and pressure work as estimated by ventricular pressure, are impaired when myocardial contraction is compromised. At times, diastolic function, assessed by ventricular relaxation and filling, is impaired. In addition to the dysfunction that occurs, there is a longer term response of the myocardium to sepsis, and this response is similar to that which is elicited in the heart by multiple brief ischemia/reperfusion episodes and by numerous pharmacological agents as well as heat stress and modified forms of lipopolysaccharide. The myocardium develops protection after an initial stress such that during a second stress, the myocardium does not exhibit as much damage as does a non-protected heart. Many agents can induce this protection which has been termed preconditioning. Both early preconditioning (protection that is measurable min to hours after the initial stimulus) and late preconditioning (protection that is measurable hours to days after the initial

Changing axis deviation during acute myocardial infarction.

PubMed

Patanè, Salvatore; Marte, Filippo

2010-07-09

Changing axis deviation has been reported during acute myocardial infarction also associated with atrial fibrillation. Isolated left posterior hemiblock is a very rare finding but the evidence of transient right axis deviation with a left posterior hemiblock pattern has been reported during acute anterior myocardial infarction as related with significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery. We present a case of changing axis deviation in a 70-year-old Italian man with acute myocardial infarction. Copyright (c) 2008 Elsevier Ireland Ltd. All rights reserved.

Acute impairment of regional myocardial glucose uptake in the apical ballooning (takotsubo) syndrome.

PubMed

Bybee, Kevin A; Murphy, Joseph; Prasad, Abhiram; Wright, R Scott; Lerman, Amir; Rihal, Charanjit S; Chareonthaitawee, Panithaya

2006-01-01

Apical ballooning syndrome (ABS) is a poorly understood clinical entity characterized by acute, transient systolic dysfunction of the left ventricular (LV) apex in the absence of epicardial coronary artery disease and commonly associated with acute emotional stress. We report abnormal regional myocardial perfusion and glucose uptake in 4 consecutive ABS patients studied using positron emission tomography with 13N-ammonia and 18F-fluorodeoxyglucose within 72 hours of presentation with ABS. All patients were postmenopausal females, 3 of whom had a major recent life stress event. Coronary angiography revealed no or minimal obstructive epicardial coronary artery disease. All patients exhibited reduced glucose uptake in the mid-LV and apical myocardial segments, which was out of proportion to perfusion abnormalities in half of the cases. In all 4 patients, affected regions subsequently recovered regional LV systolic function within 6 weeks.

Regional myocardial extraction of a radioiodinated branched chain fatty acid during right ventricular pressure overload due to acute pulmonary hypertension

DOE Office of Scientific and Technical Information (OSTI.GOV)

Hurford, W.; Lowenstein, E.; Zapol, W.

1985-05-01

To determine whether branched chain fatty acid extraction is reduced during right ventricular (RV) dysfunction due to acute pulmonary artery hypertension, studies were done in 6 anesthetized dogs. Regional branched chain fatty acid extraction was measured by comparing the myocardial uptake of I-125 labeled 15-(p-(iodophenyl))-3-methylpentadecanoic acid (I-PDA) to myocardial blood flow. Acute pulmonary hypertension was induced by incremental intravenous injection of 100 micron diameter glass beads into six pentobarbital anesthetized, mechanically ventilated dogs. Myocardial blood flow was measured by radiolabeled microspheres both under baseline conditions and during pulmonary hypertension. Mean RV pressure rose from 12 +- 2 (mean +- SEM)more » to 30 +-3mmHg resulting in a 225 +- 16% increase in RV stroke work. RV ejection fraction, as assessed by gated blood pool scans fell from 39 +- 2 to 18 +- 2%. Left ventricular (LV) pressures, stroke work and ejection fraction were unchanged. Myocardial blood flow increased 132 + 59% in the RV free wall and 67 +- 22% in the RV septum. LV blood flow was unchanged. Despite increased RV work and myocardial blood flow, no differences were noted in the branched chain fatty acid extraction ratios among LV or RV free walls or septum. The authors conclude that early RV dysfunction associated with pulmonary artery hypertension is not due to inadequate myocardial blood flow or branched chain fatty acid extraction.« less

Transmyocardial laser revascularization in the acute ischaemic heart: no improvement of acute myocardial perfusion or prevention of myocardial infarction.

PubMed

Eckstein, F S; Scheule, A M; Vogel, U; Schmid, S T; Miller, S; Jurmann, M J; Ziemer, G

1999-05-01

Transmyocardial laser revascularization (TMLR) has been used to provide enhanced myocardial perfusion in patients not suitable for coronary revascularization or angioplasty. This study investigates the acute changes in myocardial perfusion after TMLR with a Holmium:Yttrium-Aluminium-Garnet (YAG) laser with a thermal imaging camera in a model of acute ischaemia, and confirms its midterm effects by post-mortem investigation of magnetic resonance imaging and histopathological examination. Acute myocardial ischaemia was induced by occlusion of the dominant diagonal branch in ten sheep. Perfusion measurements were undertaken first in the unaffected myocardium, then after temporary occlusion of the coronary to obtain a control measurement for ischaemic myocardium. Myocardial perfusion was then evaluated during reperfusion after release of coronary occlusion. Then the coronary was permanently occluded and 20.5+/-2 channels were drilled with the Holmium:YAG laser and perfusion was measured again. The other four sheep served as control with untreated ischaemia. All animals were sacrificed after 28 days following administration of gadolinium i.v. to serve as contrast medium for magnetic resonance tomography. The hearts were subjected to magnetic resonance tomography and histopathological examination. Intraoperative perfusion measurements revealed a decreased perfusion after temporary occlusion and an increased perfusion in reperfused myocardium. After TMLR, no improvement of myocardial perfusion above the ischaemic level could be shown. Magnetic resonance images could neither confirm patent laser channels nor viable myocardium within ischaemic areas. On histology no patent endocardial laser channel could be detected. The transmural features were myocardial infarct with scar tissue. In the presented sheep model with acute ischaemia, TMLR with a Holmium:YAG laser did not provide acute improvement of myocardial perfusion as assessed by a thermal imaging camera. This would

Diabetes Mellitus and Cardiogenic Shock Complicating Acute Myocardial Infarction.

PubMed

Echouffo-Tcheugui, Justin B; Kolte, Dhaval; Khera, Sahil; Aronow, Herbert D; Abbott, J Dawn; Bhatt, Deepak L; Fonarow, Gregg C

2018-03-27

Diabetes mellitus (diabetes) increases the risk of acute myocardial infarction, which can result in cardiogenic shock. Data on the relation of diabetes and the occurrence and prognosis of cardiogenic shock postacute myocardial infarction are scant. Among the National Inpatient Sample patients aged ≥18 years and hospitalized for acute myocardial infarction during the 2012-2014 period, we examined the association between diabetes and the incidence and outcomes of cardiogenic shock complicating acute myocardial infarction, using multivariable logistic and linear regression models. Of 1,332,530 hospitalizations for acute myocardial infarction, 72,765 (5.5%) were complicated by cardiogenic shock. In acute myocardial infarction patients, cardiogenic shock incidence was higher among those with vs without diabetes (5.8% vs 5.2%; adjusted odds ratio [aOR] 1.14; 95% confidence interval [CI], 1.11-1.19; P < .001), with 42.8% (n = 31,135) of patients with acute myocardial infarction and cardiogenic shock having diabetes. Diabetic patients were less likely to undergo revascularization (percutaneous coronary intervention or coronary artery bypass grafting) (67.1% vs 68.7%; aOR 0.88; 95% CI, 0.80-0.96; P = .003). Diabetes was associated with higher in-hospital mortality in patients with acute myocardial infarction and cardiogenic shock (37.9% vs 36.8%; aOR 1.18; 95% CI, 1.09-1.28; P < .001). Among survivors, patients with diabetes had a longer hospital stay (mean ± SEM: 11.6 ± 0.16 vs 10.9 ± 0.16 days; adjusted estimate 1.12; 95% CI, 1.06-1.18; P < .001) and were more likely to be discharged to a skilled nursing home or with home health care (56.0% vs 50.5%; aOR 1.19; 95% CI, 1.07-1.33; P = .001). In a large cohort of acute myocardial infarction patients, preexisting diabetes was associated with an increased risk of cardiogenic shock and worse outcomes in those with cardiogenic shock. Copyright © 2018 Elsevier Inc. All rights reserved.

Acute myocardial infarction mortality in Cuba, 1999-2008.

PubMed

Armas, Nurys B; Ortega, Yanela Y; de la Noval, Reinaldo; Suárez, Ramón; Llerena, Lorenzo; Dueñas, Alfredo F

2012-10-01

Acute myocardial infarction is one of the leading causes of death in the world. This is also true in Cuba, where no national-level epidemiologic studies of related mortality have been published in recent years. Describe acute myocardial infarction mortality in Cuba from 1999 through 2008. A descriptive study was conducted of persons aged ≥25 years with a diagnosis of acute myocardial infarction from 1999 through 2008. Data were obtained from the Ministry of Public Health's National Statistics Division database for variables: age; sex; site (out of hospital, in hospital or in hospital emergency room) and location (jurisdiction) of death. Proportions, age- and sex-specific rates and age-standardized overall rates per 100,000 population were calculated and compared over time, using the two five-year time frames within the study period. A total of 145,808 persons who had suffered acute myocardial infarction were recorded, 75,512 of whom died, for a case-fatality rate of 51.8% (55.1% in 1999-2003 and 49.7% in 2004-2008). In the first five-year period, mortality was 98.9 per 100,000 population, falling to 81.8 per 100,000 in the second; most affected were people aged ≥75 years and men. Of Cuba's 14 provinces and special municipality, Havana, Havana City and Camagüey provinces, and the Isle of Youth Special Municipality showed the highest mortality; Holguín, Ciego de Ávila and Granma provinces the lowest. Out-of-hospital deaths accounted for the greatest proportion of deaths in both five-year periods (54.8% and 59.2% in 1999-2003 and 2004-2008, respectively). Although risk of death from acute myocardial infarction decreased through the study period, it remains a major health problem in Cuba. A national acute myocardial infarction case registry is needed. Also required is further research to help elucidate possible causes of Cuba's high acute myocardial infarction mortality: cardiovascular risk studies, studies of out-of-hospital mortality and quality of care

Current trend of acute myocardial infarction in Korea (from the Korea Acute Myocardial Infarction Registry from 2006 to 2013).

PubMed

Kook, Hyun Yi; Jeong, Myung Ho; Oh, Sangeun; Yoo, Sung-Hee; Kim, Eun Jung; Ahn, Youngkeun; Kim, Ju Han; Chai, Leem Soon; Kim, Young Jo; Kim, Chong Jin; Chan Cho, Myeong

2014-12-15

Although the incidence of acute myocardial infarction (AMI) in Korea has been rapidly changed because of westernization of diet, lifestyle, and aging of the population, the recent trend of the myocardial infarction have not been reported by classification. We investigated recent trends in the incidence and mortality associated with the 2 major types of AMI. We reviewed 39,978 patients registered in the Korea Acute Myocardial Infarction Registry for either ST-segment elevation acute myocardial infarction (STEMI) or non-ST-segment elevation acute myocardial infarction (NSTEMI) from 2006 to 2013. When the rate for AMI were investigated according to each year, the incidence rates of STEMI decreased markedly from 60.5% in 2006 to 48.1% in 2013 (p <0.001). In contrast, a gradual increase in the incidence rates of NSTEMI was observed from 39.5% in 2006 to 51.9% in 2013 (p <0.001). As risk factors, hypertension, diabetes mellitus, and dyslipidemia were much more common in patients with NSTEMI than STEMI. Among medical treatments, the use of β blockers, angiotensin receptor blocker, and statin were increased from 2006 to 2013 in patients with STEMI and NSTEMI. Patients with STEMI and NSTEMI were more inclined to be increasingly treated by invasive treatments with percutaneous coronary intervention. In conclusion, this study demonstrated that the trend of myocardial infarction has been changed rapidly in the aspect of risk factors, ratio of STEMI versus NSTEMI, and therapeutic strategies during the recent 8 years in Korea. Copyright © 2014 Elsevier Inc. All rights reserved.

Diagnosis of acute myocardial infarction.

PubMed

Pandey, Rudradev; Gupta, Naveen K; Wander, Gurpreet S

2011-12-01

Diagnosis of acute myocardial infarction (AMI) has to be made early in the emergency triage since maximal mortality occurs within first hour and the benefits of all interventions are greater once these are instituted early. Diagnosis is easy and based on simple principals of good history, physical examination, early and complete 12 lead electrocardiogram and use of echocardiography which should be available in the emergency triage area. Subsequently biomarkers are also available for documentation and risk stratification. The other causes of acute severe chest pain should be kept in mind and ruled out. The role of myocardial perfusion imaging for diagnosis of AMI is limited. The diagnosis also involves an estimation of the size of infarct, duration since onset of the process, any acute complications of AMI and the likely vessel involved since these have significant therapeutic implications.

An Unusual Complication Following Transarterial Chemoembolization: Acute Myocardial Infarction

DOE Office of Scientific and Technical Information (OSTI.GOV)

Lai Yiliang; Chang Weichou; Kuo Wuhsien

Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellularmore » carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.« less

Prostate-specific antigen and acute myocardial infarction: a possible new intriguing scenario.

PubMed

Patanè, Salvatore; Marte, Filippo

2009-05-29

Prostate-specific antigen (PSA) has been identified as a member of the human kallikrein family of serine proteases and it is an established marker for detection of prostate cancer. Apparently spurious result has been reported in a work about mean serum PSA concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. Elevation of prostate-specific antigen has also been reported during acute myocardial infarction in three patients and in another one also after transurethral resection of the prostate (TURP) and without histological diagnosis of prostate cancer. In our report we present three cases of diminution of serum PSA concentration during acute myocardial infarction. Our report extends the evaluation of PSA during acute myocardial infarction. It seems that when elevation of prostate-specific antigen occurs during acute myocardial infarction, coronary lesions are frequent and often more severe than when diminution of prostate-specific antigen occurs during acute myocardial infarction. It opens a possible new intriguing scenario of the role of the prostate-specific antigen in acute myocardial infarction.

B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction.

PubMed

Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

2013-10-01

Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6C(hi) monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell-selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction.

B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

PubMed Central

Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

2014-01-01

Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6Chi monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell–selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction. PMID:24037091

Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers

ClinicalTrials.gov

2017-12-08

Acute Myocardial Infarction (AMI); Acute Coronary Syndrome (ACS); ST Elevation (STEMI) Myocardial Infarction; Ischemic Reperfusion Injury; Non-ST Elevation (NSTEMI) Myocardial Infarction; Angina, Unstable

Biventricular assist device for scombroid poisoning with refractory myocardial dysfunction: a bridge to recovery.

PubMed

Grinda, Jean-Michel; Bellenfant, Florence; Brivet, François Gilles; Carel, Yvan; Deloche, Alain

2004-09-01

We report the usefulness of biventricular mechanical circulatory support in a 36-yr-old woman with refractory myocardial dysfunction resulting from scombroid poisoning. Case report. Medical and surgical university care units. A previously healthy 36-yr-old woman with severe myocardial dysfunction unresponsive to epinephrine (1.3 microg/kg/min) and dobutamine (18 microg/kg/min) after the ingestion of cooked fresh tuna. Implantation at day 3 of a biventricular assist device consisting of two paracorporeal pneumatic pumps set at 70 beats/min to reach an output of 5.6 L/min during 8 days. The biventricular mechanical circulatory assist device allowed weaning of the inotropic drugs, maintenance of end-organ function, and support of the patient until myocardial recovery. The patient was successfully explanted 11 days after ingestion. Cardiac function had totally recovered, but a stroke was noted. At 3-yrs follow-up, there was no cardiac or neurologic sequela. This report describes severe myocardial dysfunction secondary to scombroid poisoning and demonstrates the usefulness of a mechanical circulatory assist device as a bridge to recovery.

[Acute myocardial infarction in Morocco: FES-AMI registry data].

PubMed

Akoudad, H; El Khorb, N; Sekkali, N; Mechrafi, A; Zakari, N; Ouaha, L; Lahlou, I

2015-12-01

Acute myocardial infarction is the most dangerous complication of coronary atherothrombosis. There are several disparities in regard to its management around the world. The aim of this study is to analyze the specificities of management of acute myocardial infarction in Morocco. FES-AMI (Fès Acute Myocardial Infarction) is a prospective monocentric registry conducted in cardiology department of Hassan II university hospital in Fès. In this registry, we enrolled patients with acute myocardial infarction who presented within 5 days after symptom onset. From January 2005 to August 2015, we enrolled 1835 patients. Seventy-five percent of patients were males and mean age was 60 years old. Fifty-one percent of patients were smokers, 27% were hypertensives and 14% were diabetics. Sixty-six percent of patients had more than 2 risk factors. Time from symptom onset to hospital admission was less than six hours for 40% of the patients. Thirty-six percent of patients were admitted more than twelve hours after the onset of chest pain. Only 37% of patients received reperfusion therapy, 31% with in-hospital thrombolysis and 6% with primary angioplasty. In-hospital mortality was 7.6%. The patients enrolled in our registry have late presentation of acute myocardial infarction and less rate of reperfusion therapy. Furthermore, the majority of our patients have multiple risk factors and this result underlines the failure of preventive interventions. Copyright © 2015 Elsevier Masson SAS. All rights reserved.

A History of Streptokinase Use in Acute Myocardial Infarction

PubMed Central

Sikri, Nikhil; Bardia, Amit

2007-01-01

A serendipitous discovery by William Smith Tillett in 1933, followed by many years of work with his student Sol Sherry, laid a sound foundation for the use of streptokinase as a thrombolytic agent in the treatment of acute myocardial infarction. The drug found initial clinical application in combating fibrinous pleural exudates, hemothorax, and tuberculous meningitis. In 1958, Sherry and others started using streptokinase in patients with acute myocardial infarction and changed the focus of treatment from palliation to “cure.” Initial trials that used streptokinase infusion produced conflicting results. An innovative approach of intracoronary streptokinase infusion was initiated by Rentrop and colleagues in 1979. Subsequently, larger trials of intracoronary infusion achieved reperfusion rates ranging from 70% to 90%. The need for a meticulously planned and systematically executed randomized multicenter trial was fulfilled by the Gruppo Italiano per la Sperimentazione della Streptochinasi nell'Infarto Miocardico (GISSI) trial in 1986, which not only validated streptokinase as an effective therapeutic method but also established a fixed protocol for its use in acute myocardial infarction. Currently, despite the wide use of tissue plasminogen activator in developed nations, streptokinase remains essential to the management of acute myocardial infarction in developing nations. PMID:17948083

Evaluation of cerebral-cardiac syndrome using echocardiography in a canine model of acute traumatic brain injury.

PubMed

Qian, Rong; Yang, Weizhong; Wang, Xiumei; Xu, Zhen; Liu, Xiaodong; Sun, Bing

2015-01-01

Previous studies have confirmed that traumatic brain injury (TBI) can induce general adaptation syndrome (GAS), which subsequently results in myocardial dysfunction and damage in some patients with acute TBI; this condition is also termed as cerebral-cardiac syndrome. However, most clinicians ignore the detection and treatment of myocardial dysfunction, and instead concentrate only on the serious neural damage that is observed in acute TBI, which is one of the most important fatal factors. Therefore, clarification is urgently needed regarding the relationship between TBI and myocardial dysfunction. In the present study, we evaluated 18 canine models of acute TBI, by using real-time myocardial contrast echocardiography and strain rate imaging to accurately evaluate myocardial function and regional microcirculation, including the strain rate of the different myocardial segments, time-amplitude curves, mean ascending slope of the curve, and local myocardial blood flow. Our results suggest that acute TBI often results in cerebral-cardiac syndrome, which rapidly progresses to the serious stage within 3 days. This study is the first to provide comprehensive ultrasonic characteristics of cerebral-cardiac syndrome in an animal model of TBI.

Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction.

PubMed

Wang, Wei; Zhang, Fuyang; Xia, Yunlong; Zhao, Shihao; Yan, Wenjun; Wang, Helin; Lee, Yan; Li, Congye; Zhang, Ling; Lian, Kun; Gao, Erhe; Cheng, Hexiang; Tao, Ling

2016-11-01

Cardiac metabolic remodeling is a central event during heart failure (HF) development following myocardial infarction (MI). It is well known that myocardial glucose and fatty acid dysmetabolism contribute to post-MI cardiac dysfunction and remodeling. However, the role of amino acid metabolism in post-MI HF remains elusive. Branched chain amino acids (BCAAs) are an important group of essential amino acids and function as crucial nutrient signaling in mammalian animals. The present study aimed to determine the role of cardiac BCAA metabolism in post-MI HF progression. Utilizing coronary artery ligation-induced murine MI models, we found that myocardial BCAA catabolism was significantly impaired in response to permanent MI, therefore leading to an obvious elevation of myocardial BCAA abundance. In MI-operated mice, oral BCAA administration further increased cardiac BCAA levels, activated the mammalian target of rapamycin (mTOR) signaling, and exacerbated cardiac dysfunction and remodeling. These data demonstrate that BCAAs act as a direct contributor to post-MI cardiac pathologies. Furthermore, these BCAA-mediated deleterious effects were improved by rapamycin cotreatment, revealing an indispensable role of mTOR in BCAA-mediated adverse effects on cardiac function/structure post-MI. Of note, pharmacological inhibition of branched chain ketoacid dehydrogenase kinase (BDK), a negative regulator of myocardial BCAA catabolism, significantly improved cardiac BCAA catabolic disorders, reduced myocardial BCAA levels, and ameliorated post-MI cardiac dysfunction and remodeling. In conclusion, our data provide the evidence that impaired cardiac BCAA catabolism directly contributes to post-MI cardiac dysfunction and remodeling. Moreover, improving cardiac BCAA catabolic defects may be a promising therapeutic strategy against post-MI HF. Copyright © 2016 the American Physiological Society.

The association of ventricular tachycardia and endothelial dysfunction in the setting of acute myocardial infarction with ST elevation

PubMed Central

Škerk, Vedrana; Markotić, Alemka; Brkljačić, Diana Delić; Manola, Šime; Krčmar, Tomislav; Gabrić, Ivo Darko; Štajminger, Gordana; Pintarić, Hrvoje

2013-01-01

Background Ventricular tachycardia (VT) is frequently seen in ischemic settings like acute myocardial infarction with ST segment elevation (STEMI). Endothelial dysfunction (ED) represents inflammation and the loss of all protective features of the endothelium. We aimed to examine the association between VT and ED in patients with STEMI. Material/Methods The study included 90 subjects (30 with VT and acute STEMI, 30 with STEMI without VT, and 30 controls). Sera of all subjects were tested on ED markers by enzyme immunoassay: sICAM-1 (intracellular adhesive molecule-1), sVCAM-1 (vascular adhesive molecule-1), P- and E-selectins, and VEGF (vascular endothelial growth factor). In addition, CRP (C-reactive protein) was detected. Results Significantly increased values of low-density lipoprotein, triglycerides, leukocytes, creatinine, and the number of cigarettes smoked were observed among patients with VT+STEMI in comparison to controls. The levels of E-selectin were significantly lower in the VT+STEMI group than in the other groups, while the levels of VCAM-1 were significantly higher in the groups with STEMI and VT+STEMI compared to the controls. Lower levels of VEGF were recorded in STEMI and VT+STEMI groups compared to the control group. A significant correlation between CRP and VCAM-1 in patients with VT +STEMI was demonstrated. Conclusions We showed that ED may have a role in the immunopathogenesis of VT in patients with STEMI. The role of sE-selectin and correlation of sVCAM-1 with CRP as possible ED predictive markers in patients with VT+STEMI should be further investigated in a large cohort of patients. PMID:24253420

Single High-Sensitivity Cardiac Troponin I to Rule Out Acute Myocardial Infarction.

PubMed

Sandoval, Yader; Smith, Stephen W; Love, Sara A; Sexter, Anne; Schulz, Karen; Apple, Fred S

2017-09-01

This study examined the performance of single high-sensitivity cardiac troponin I (hs-cTnI) measurement strategies to rule out acute myocardial infarction. This was a prospective, observational study of consecutive patients presenting to the emergency department (n = 1631) in whom cTnI measurements were obtained using an investigational hs-cTnI assay. The goals of the study were to determine 1) negative predictive value (NPV) and sensitivity for the diagnosis of acute myocardial infarction, type 1 myocardial infarction, and type 2 myocardial infarction; and 2) safety outcome of acute myocardial infarction or cardiac death at 30 days using hs-cTnI less than the limit of detection (LoD) (<1.9 ng/L) or the High-STEACS threshold (<5 ng/L) alone and in combination with normal electrocardiogram (ECG). Acute myocardial infarction occurred in 170 patients (10.4%), including 68 (4.2%) type 1 myocardial infarction and 102 (6.3%) type 2 myocardial infarction. For hs-cTnIacute myocardial infarction were 99.6% (95% confidence interval 98.9%-100%) and 98.8 (97.2%-100%). For hs-cTnI<5 ng/L (50%), the NPV and sensitivity for acute myocardial infarction were 98.9% (98.2%-99.6%) and 94.7% (91.3%-98.1%). In combination with a normal ECG, 1) hs-cTnIacute myocardial infarction and who are at very low risk for adverse events at 30 days. Copyright © 2017 Elsevier Inc. All rights reserved.

Does overprotection cause cardiac invalidism after acute myocardial infarction?

PubMed

Riegel, B J; Dracup, K A

1992-01-01

To determine if overprotection on the part of the patient's family and friends contributes to the development of cardiac invalidism after acute myocardial infarction. Longitudinal survey. Nine hospitals in the southwestern United States. One hundred eleven patients who had experienced a first acute myocardial infarction. Subjects were predominantly male, older-aged, married, caucasian, and in functional class I. Eighty-one patients characterized themselves as being overprotected (i.e., receiving more social support from family and friends than desired), and 28 reported receiving inadequate support. Only two patients reported receiving as much support as they desired. Self-esteem, emotional distress, health perceptions, interpersonal dependency, return to work. Overprotected patients experienced less anxiety, depression, anger, confusion, more vigor, and higher self-esteem than inadequately supported patients 1 month after myocardial infarction (p < 0.05). Inadequately supported patients were more dependent 4 months after the event. Overprotection on the part of family and friends may facilitate psychosocial adjustment in the early months after an acute myocardial infarction rather than lead to cardiac invalidism.

In vivo characterization of acute myocardial ischemia using photoacoustic imaging with a focused transducer

NASA Astrophysics Data System (ADS)

Li, Zhifang; Chen, Haiyu; Xie, Wengming; Li, Hui

2011-03-01

We explore the feasibility of using photoacoustic imaging based on a focused transducer to characterizing acute myocardial ischemia at different stage. In this study, we blocked rat left anterior coronary descending artery (LAD) to induce the acute myocardial ischemia. The results show that the intensity and areas of photoacoustic images of myocardial decrease with the LAD time increasing, which suggests that photoacoustic imaging has a potential for diagnosis of acute myocardial ischemia.

Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues

PubMed Central

Zhou, Hourong; Huang, Jia; Zhu, Li; Cao, Yu

2018-01-01

Activation of renin-angiotensin system (RAS) is one of the pathological mechanisms associated with myocardial ischemia-reperfusion injury following resuscitation. The present study aimed to determine whether erythropoietin (EPO) improves post-resuscitation myocardial dysfunction and how it affects the renin-angiotensin system. Sprague-Dawley rats were randomly divided into sham, vehicle, epinephrine (EP), EPO and EP + EPO groups. Excluding the sham group, all groups underwent cardiopulmonary resuscitation (CPR) 4 min after asphyxia-induced cardiac arrest (CA). EP and/or EPO was administrated by intravenous injection when CPR began. The results demonstrated that the vehicle group exhibited lower mean arterial pressure, left ventricular systolic pressure, maximal ascending rate of left ventricular pressure during left ventricular isovolumic contraction and maximal descending rate of left ventricular pressure during left ventricular isovolumic relaxation (+LVdP/dt max and -LVdP/dt max, respectively), and higher left ventricular end-diastolic pressure, compared with the sham group following return of spontaneous circulation (ROSC). Few significant differences were observed concerning the myocardial function between the vehicle and EP groups; however, compared with the vehicle group, EPO reversed myocardial function indices following ROSC, excluding-LVdP/dt max. Serum renin and angiotensin (Ang) II levels were measured by ELISA. The serum levels of renin and Ang II were significantly increased in the vehicle group compared with the sham group, which was also observed for the myocardial expression of renin and Ang II receptor type 1 (AT1R), as determined by reverse transcription-quantitative polymerase chain reaction and western blotting. EPO alone did not significantly reduce the high serum levels of renin and Ang II post-resuscitation, but changed the protein levels of renin and AT1R expression in myocardial tissues. However, EPO enhanced the myocardial expression of

Influence of climate variability on acute myocardial infarction mortality in Havana, 2001-2012.

PubMed

Rivero, Alina; Bolufé, Javier; Ortiz, Paulo L; Rodríguez, Yunisleydi; Reyes, María C

2015-04-01

Death from acute myocardial infarction is due to many factors; influences on risk to the individual include habits, lifestyle and behavior, as well as weather, climate and other environmental components. Changing climate patterns make it especially important to understand how climatic variability may influence acute myocardial infarction mortality. Describe the relationship between climate variability and acute myocardial infarction mortality during the period 2001-2012 in Havana. An ecological time-series study was conducted. The universe comprised 23,744 deaths from acute myocardial infarction (ICD-10: I21-I22) in Havana residents from 2001 to 2012. Climate variability and seasonal anomalies were described using the Bultó-1 bioclimatic index (comprising variables of temperature, humidity, precipitation, and atmospheric pressure), along with series analysis to determine different seasonal-to-interannual climate variation signals. The role played by climate variables in acute myocardial infarction mortality was determined using factor analysis. The Mann-Kendall and Pettitt statistical tests were used for trend analysis with a significance level of 5%. The strong association between climate variability conditions described using the Bultó-1 bioclimatic index and acute myocardial infarctions accounts for the marked seasonal pattern in AMI mortality. The highest mortality rate occurred during the dry season, i.e., the winter months in Cuba (November-April), with peak numbers in January, December and March. The lowest mortality coincided with the rainy season, i.e., the summer months (May-October). A downward trend in total number of deaths can be seen starting with the change point in April 2009. Climate variability is inversely associated with an increase in acute myocardial infarction mortality as is shown by the Bultó-1 index. This inverse relationship accounts for acute myocardial infarction mortality's seasonal pattern.

[Interventional therapy of acute myocardial infarction].

PubMed

Zahn, R; Zeymer, U

2008-09-01

Currently an acute myocardial infarction has to be differentiated into ST-elevation myocardial infarction (STEMI) or non ST-elevation myocardial infarction (NSTEMI). However, there exists another definition of acute coronary syndromes (ACS), which is more important in clinical practice, for all recommendations from the guidelines of the cardiac societies concerning the invasive strategies rely on this one. Here one has to differentiate an ACS with ST-elevation (STE-ACS = STEMI) from an ACS without ST-elevation (NSTE-ACS). The last one is further divided into an NSTE-ACS with or without high risk. In patients with an NSTE-ACS with high risk an early invasive strategy is recommended within 72 h after the diagnosis. In patients with an NSTE-ACS without high risk a more conservative approach can be pursued. In STE-ACS patients primary angioplasty is the reperfusion therapy of choice, if it can be performed in a timely fashion within 2 h after diagnosis at an interventional centre with experienced interventionalists and short "door-to-balloon" times. In Germany this goal is achievable almost everywhere. Therefore it is currently the most important task to establish local networks to reach this goal.

The 1999 Ji-Ji (Taiwan) earthquake as a trigger for acute myocardial infarction.

PubMed

Tsai, Ching-Hong; Lung, For-Wey; Wang, Shing-Yaw

2004-01-01

The authors evaluated the effect of stress due to the Ji-Ji, Taiwan, earthquake, which occurred at 1:47 a.m. on September 21, 1999, on the onset of acute myocardial infarction in six counties near the earthquake epicenter. The rate of hospitalization due to acute myocardial infarction increased during the 6 weeks after the earthquake, and a significantly higher number of patients were hospitalized with acute myocardial infarction during that period, compared with the same 6-week period in the previous year (99 and 65 patients, respectively). The findings suggest that extreme emotional stress due to the natural disaster, superimposed on the stress of awakening, increased the incidence of acute myocardial infarction in this population.

Symptoms of acute myocardial infarction: A correlational study of the discrepancy between patients' expectations and experiences.

PubMed

Abed, Mona A; Ali, Raeda M Abu; Abu Ras, Motaz M; Hamdallah, Faten O; Khalil, Amani A; Moser, Debra K

2015-10-01

Patients' responses to acute myocardial infarction symptoms are affected by symptom incongruence, which is the difference between the symptoms they expect to experience and the symptoms they actually experienced during an acute myocardial infarction. To examine the relationship of patients' demographics, clinical characteristics and sources of information about acute myocardial infarction with their symptom expectations, actual experiences and symptom incongruence. Descriptive correlational study. Patients were recruited from ten hospitals in the two most populated cities in Jordan (Amman and Al Zarqa). Jordanian patients with acute myocardial infarction were recruited. Inclusion criteria were age 18 years or older, diagnosis of acute myocardial infarction, oriented, mentally competent and fluent in Arabic. Exclusion criteria were experiencing acute myocardial infarction during a hospitalization or having severe psychiatric illnesses. The Morgan Incongruence of Heart Attack Symptoms Index was used to quantify symptom incongruence and identify patients' expected and experienced acute myocardial infarction symptoms. Patients' information sources about acute myocardial infarction and demographic and clinical characteristics were collected by interview and medical chart review. Patients (N=299) were mostly males (80%) and married (92%). The average age was 56±12.3 years. Patients expected a limited number of acute myocardial infarction symptoms and these expectations were largely confined to typical symptoms and matched their experiences. Patients who were female, elderly, nonsmokers, poorly educated, with low income, and those who were normolipidemic, had no personal or family cardiac history, and were informed about acute myocardial infarction by relatives expected fewer symptoms (mostly typical and atypical) than their counterparts. Elderly patients and those with hyperlipidemia experienced fewer typical symptoms than their counterparts. Patients with ST

Chronic Kidney Disease and Risk of Presenting with Acute Myocardial Infarction versus Stable Exertional Angina in Adults with Coronary Heart Disease

PubMed Central

Go, Alan S.; Bansal, Nisha; Chandra, Malini; Lathon, Phenius V.; Fortmann, Stephen P.; Iribarren, Carlos; Hsu, Chi-yuan; Hlatky, Mark A.

2011-01-01

Objective To examine whether kidney dysfunction is associated with the type of clinical presentation of coronary heart disease (CHD). Background Reduced kidney function increases risk of developing CHD, but it is not known whether it also influences the acuity of clinical presentation, which has important prognostic implications. Methods We conducted a case-control study of subjects whose first clinical presentation of CHD was either acute myocardial infarction or stable exertional angina between October 2001-December 2003. Glomerular filtration rate (eGFR) before the incident event was estimated using calibrated serum creatinine and the abbreviated MDRD equation. Patient characteristics and use of medications were ascertained from self-report and health plan databases. We used multivariable logistic regression to examine the association of reduced eGFR and CHD presentation. Results We studied 803 adults with incident acute myocardial infarction and 419 adults with incident stable exertional angina who had a baseline eGFR ≤130 ml/min/1.73 m2. Mean eGFR was lower among subjects with acute myocardial infarction compared with stable angina. Compared with eGFR 90–130 ml/min/1.73 m2, we found a strong, graded independent association between reduced eGFR and presenting with acute myocardial infarction: adjusted odds ratio (OR) 1.36 (95% CI: 0.99 to 1.86) for eGFR 60–89 ml/min/1.73 m2, OR 1.55 (0.92 to 2.62) for eGFR 45–59 ml/min/1.73 m2 and OR 3.82 (1.55 to 9.46) for eGFR <45 ml/min/1.73 m2 (P<0.001 for trend). Conclusion eGFR less than 45 ml/min/1.73 m2 is a strong, independent predictor of presenting with acute myocardial infarction versus stable angina as the initial manifestation of CHD. PMID:21958887

Decision making processes in people with symptoms of acute myocardial infarction: qualitative study

PubMed Central

Pattenden, Jill; Watt, Ian; Lewin, Robert J P; Stanford, Neil

2002-01-01

Objective To identify the themes that influence decision making processes used by patients with symptoms of acute myocardial infarction. Design Qualitative study using semistructured interviews. Setting Two district hospitals in North Yorkshire. Participants 22 patients admitted to hospital with confirmed second, third, or fourth acute myocardial infarction. Main outcome measure Patients' perceptions of their experience between the onset of symptoms and the decision to seek medical help. Results Six main themes that influence the decision making process were identified: appraisal of symptoms, perceived risk, previous experience, psychological and emotional factors, use of the NHS, and context of the event. Conclusions Knowledge of symptoms may not be enough to promote prompt action in the event of an acute myocardial infarction. Cognitive and emotional processes, individual beliefs and values, and the influence of the context of the event should also be considered in individual interventions designed to reduce delay in the event of symptoms of acute myocardial infarction. What is already known on this topicIndividual sociodemographic and clinical characteristics affect the time to seeking medical care in patients with symptoms of acute myocardial infarctionAppraisal of symptoms is difficult; people with classic and severe symptoms are more likely to take prompt actionWhat this study addsThe decision to seek medical help in patients who have had one or more previous myocardial infarctions is a complex processSimply providing patients with information on symptoms of acute myocardial infarction, and what to do in the event of these symptoms, may not be sufficient to promote prompt action PMID:11976241

Multislice coronary computed tomographic angiography in emergency department presentations of unsuspected acute myocardial infarction.

PubMed

Hecht, Harvey S; Bhatti, Tandeep

2009-01-01

Coronary computed tomographic angiography (CCTA) is not indicated in the setting of acute myocardial infarction in the emergency department (ED). Nonetheless, acute coronary syndromes may have atypical presentations, and CCTA may be inadvertently performed in this setting. This study was designed to determine the frequency and characteristics of CCTA imaging of unsuspected acute myocardial infarction in the ED. All CCTAs performed in the ED at Lenox Hill Hospital were reviewed for clinical indications and subsequent course; patients with documented acute myocardial infarction were identified. Of the 500 CCTAs performed on ED patients in the Lenox Hill laboratory, 5 patients (1%) were imaged during the initial phase of an unsuspected acute myocardial infarction; in all cases the CCTAs were key to the diagnosis. The imaging characteristics were (1) total or subtotal occlusion and (2) transmural hypodensity in the infarct area. Although acute myocardial infarction on CCTA in ED patients is an infrequent event, proper and prompt recognition is critical for appropriate patient care, particularly as applications to the ED increase.

Correlation of platelet count and acute ST-elevation in myocardial infarction.

PubMed

Paul, G K; Sen, B; Bari, M A; Rahman, Z; Jamal, F; Bari, M S; Sazidur, S R

2010-07-01

The role of platelets in the pathogenesis of ST-elevation myocardial infarction (STEMI) has been substantiated by studies that demonstrated significant clinical benefits associated with antiplatelet therapy. Initial platelet counts in Acute Myocardial Infarction (AMI) may be a useful adjunct for identifying those patients who may or may not respond to fibrinolytic agents. Patient with acute STEMI has variable level of platelet count and with higher platelet count have poor in hospital outcome. There are many predictors of poor outcome in Acute Myocardial Infarction (AMI) like cardiac biomarkers (Troponin I, Troponin T and CK-MB), C-Reactive Protien (CRP) and WBC (White Blood Cell) counts. Platelet count on presentation of STEMI is one of them. Higher platelet count is associated with higher rate of adverse clinical outcome in ST-Elevation Myocardial Infarction (STEMI), like heart failure, arrhythmia, re-infarction & death. So, categorization of patient with STEMI on the basis of platelet counts may be helpful for risk stratification and management of these patients.

[Reduction of in-hospital mortality and improved secondary prevention after acute myocardial infarction. First results from the registry of secondary prevention after acute myocardial infarction (SAMI)].

PubMed

Tebbe, U; Messer, C; Stammwitz, E; The, G S; Dietl, J; Bischoff, K-O; Schulten-Baumer, U; Tebbenjohanns, J; Gohlke, H; Bramlage, P

2007-07-30

In hospital mortality of acute myocardial infarction (AMI) has been reduced due to the availability of better therapeutic strategies. But there is still a gap between mortality rates in randomised trials and daily clinical practice. Thus, it was aim of the present registry to document the course and outcome of patients with AMI and to improve patient care by implementing recent guidelines. In a nationwide registry study in hospitals in Germany with a cardiology unit or an internal medicine department data on consecutive patients were recorded for six to twelve months at admission, discharge and during a follow-up of one year. From 02/2003 until 10/2004 a total of 5,353 patients with acute myocardial infarction (65.7 % male, mean age of 67.6 +/- 17.7 years; 55.1 % of them with ST elevation myocardial infarction (STEMI) were included in the registry. Of the patients with STEMI, 76.6 % underwent acute intervention, 37.1 % had thrombolysis, 69.7 % percutaneous transluminal coronary angioplasty (PTCA). 40.0 % of those with non-Stemi (NSTEMI) had an acute intervention, 6.6 % thrombolysis, 73.5 % PTCA. Recommended secondary prevention consisted of ASS (93.2 %), beta-blockers (93.0 %), CSE-inhibitors (83.5 %), ACE-inhibitors (80.9 %) and clopidogrel (74.0 %). In-hospital mortality was 10.5 % (STEMI) and 7.4 % (NSTEMI). The 9 % mortality among patients with acute myocardial infarction treated in the hospitals participating in the SAMI registry is low compared to that in similar collectives. The high number of patients who had thrombofibrinolysis and coronary interventions as well as the early initiation of drug therapy contributed to these results. Medical treatment in the prehospital phase of these patients remains still insufficient and to a substantial extent contributes to the mortality of acute myocardial infarction.

Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation and oxidative stress in rat

PubMed Central

Chen, Huaguo; Xu, Yongfu; Wang, Jianzhong; Zhao, Wei; Ruan, Huihui

2015-01-01

Baicalin belongs to glucuronic acid glycosides and after hydrolysisbaicalein and glucuronic acid come into being. It has such effects as clearing heat and removing toxicity, anti-inflammation, choleresis, bringing high blood pressure down, diuresis, anti-allergic reaction and so on. In this study, we investigated whether baicalin ameliorates isoproterenol-induced acute myocardial infarction and its mechanism. Rat model of acute myocardial infarction was induced by isoproterenol. Casein kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH), cardiac troponin T (cTnT) and infarct size measurement were used to measure the protective effect of baicalin on isoproterenol-induced acute myocardial infarction. iNOS protein expression in rat was analyzed using western blot analysis. Tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), malondialdehyde (MDA) and superoxide dismutase (SOD) and caspase-3 activation levels were explored using commercial ELISA kits. In the acute myocardial infarction experiment, baicalin effectively ameliorates the level of CK, CK-MB, LDH and cTnT, reduced infarct size in acute myocardial infarction rat model. Meanwhile, treatment with baicalin effectively decreased the iNOS protein expression, inflammatory factors and oxidative stresses in a rat model of acute myocardial infarction. However, baicalin emerged that anti-apoptosis activity and suppressed the activation of caspase-3 in a rat model of acute myocardial infarction. The data suggest that the protective effect of baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation and oxidative stress in rat. PMID:26617721

Gender differences in physical activity following acute myocardial infarction in adults: A prospective, observational study.

PubMed

Minges, Karl E; Strait, Kelly M; Owen, Neville; Dunstan, David W; Camhi, Sarah M; Lichtman, Judith; Geda, Mary; Dreyer, Rachel P; Bueno, Héctor; Beltrame, John F; Curtis, Jeptha P; Krumholz, Harlan M

2017-01-01

Aims Despite the benefits of regular physical activity participation following acute myocardial infarction, little is known about gender differences in physical activity among patients after acute myocardial infarction. We described, by gender, physical activity trajectories pre- and post-acute myocardial infarction, and determined whether gender was independently associated with physical activity. Methods and results The Variation in Recovery: Role of Gender on Outcomes of Young AMI patients (VIRGO) study, conducted at 103 US, 24 Spanish, and three Australian hospitals, was designed, in part, to evaluate gender differences in lifestyle behaviors following acute myocardial infarction. We used baseline, one-month, and 12-month data collected from patients aged 18-55 years ( n = 3572). Patients were assigned to American Heart Association-defined levels of physical activity. A generalized estimating equation model was used to account for repeated measures within the same individual over time. Men were more active (≥150 min/wk moderate or ≥75 min/wk vigorous activity) than women at baseline (42% vs 34%), one month (45% vs 34%), and 12 months (48% vs 36%) (all p < 0.0001). Men engaged in a significantly longer duration of activity at each time point. When controlling for all other factors, women had 1.37 times the odds of being less active than men from pre-acute myocardial infarction to 12-months post-acute myocardial infarction (95% confidence interval: 1.21-1.55). Non-white race, non-active workplaces, smoking, diabetes, hypertension, and obesity were also associated independently with being less active over time (all p < 0.05). Conclusions Although activity increased modestly over time, women recovering from acute myocardial infarction were less likely to meet physical activity recommendations than were men. By identifying factors associated with low levels of activity during acute myocardial infarction recovery, targeted interventions can be

Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice.

PubMed

Fiechter, Danielle; Kats, Suzanne; Brands, Ruud; van Middelaar, Ben; Pasterkamp, Gerard; de Kleijn, Dominique; Seinen, Willem

2011-10-01

There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction. Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood. Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group. In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction.

Myocardial viability assessment after acute myocardial infarction: low-dose dobutamine echocardiography versus rest-redistribution thallium-201 SPECT.

PubMed

Castini, D; Bestetti, A; Garbin, M; Di Leo, C; Bigi, R; Sponzilli, C; Concardi, G; Gioventù, M; Tarolo, G L; Lombardi, F; Fiorentini, C

1999-09-01

The presence of tissue viability is of great importance in the prognostic work-up of patients recovering from acute myocardial infarction. However, uncertainty still exists concerning the optimal tool for its assessment. The present study was undertaken in order to compare low-dose dobutamine echocardiography and rest-redistribution thallium SPECT for predicting late improvement of regional left ventricular function after acute myocardial infarction. Fifteen patients undergoing coronary angiography, low-dose dobutamine echocardiography and rest-redistribution thallium SPECT after thrombolyzed anterior acute myocardial infarction were studied. A 3 month follow-up echocardiogram was performed in all patients and 9 underwent coronary revascularization. A significant (> or = 70%) residual stenosis of the infarct-related artery was present in 14 patients, whilst a total occlusion was observed in 1. At 3 month follow-up, 41% of the dyssynergic segments improved. The sensitivity, specificity and accuracy for late wall motion improvement was 61, 89 and 77% for low-dose dobutamine echocardiography and, respectively, 76, 45 and 58% for rest-redistribution thallium SPECT. Tissue viability was detected in 65 and 31% of dyssynergic segments by rest-redistribution thallium SPECT and low-dose dobutamine echocardiography, respectively (p < 0.001). The agreement between the two techniques was 48%. Low-dose dobutamine echocardiography is more accurate than rest-redistribution thallium SPECT for predicting 3 month wall motion improvement in patients with acute anterior myocardial infarction, mainly due to its significantly better specificity.

The influence of myocardial substrate on ventricular fibrillation waveform: A swine model of acute and postmyocardial infarction

PubMed Central

Indik, Julia H.; Donnerstein, Richard L.; Hilwig, Ronald W.; Zuercher, Mathias; Feigelman, Justin; Kern, Karl B.; Berg, Marc D.; Berg, Robert A.

2009-01-01

Objective In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods. Design An animal intervention study was conducted with comparison to a control group. Setting This study took place in a university animal laboratory. Subjects Study subjects included 37 swine. Interventions Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period. Measurements and Main Results Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten post-myocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude–spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 ± .4 Hz; lowest in acute myocardial infarction, 8.4 ± .5 Hz; and intermediate in postmyocardial infarction, 9.7 ± .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude–spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute

Phaeochromocytoma in a 86-year-old patient presenting with reversible myocardial dysfunction.

PubMed

Szwench, Elżbieta; P Czkowska, Mariola; Marczewski, Krzysztof; Klisiewicz, Anna; Micha Owska, Ilona; Ciuba, Iwona; Januszewicz, Magdalena; Prejbisz, Aleksander; Hoffman, Piotr; Januszewicz, Andrzej

2011-12-01

BACKGROUND. Phaeochromocytomas and paragangliomas are rare, mostly benign catecholamine-producing tumours of chromaffin cells of the adrenal medulla or of extra-adrenal paraganglia. Phaeochromocytoma may occur at any age, the greatest frequency being in the fourth and fifth decades. Only on extremely rare occasions does the tumour develop in the very old patients. METHODS. We are describing an 86-year-old patient with phaeochromocytoma, presenting with reversible myocardial dysfunction. RESULTS. This very old patient with phaeochromocytoma had hypertension characterized by labile blood pressure values and increased daytime blood pressure variability. This patient exhibited reversible myocardial dysfunction suggestive for "catecholaminergic cardiomyopathy", as the complication of phaeochromocytoma. After surgical removal of the tumour, recovery of left ventricular function was documented by echocardiography showing normalization of systolic function and improvement of diastolic function. CONCLUSION. Phaeochromocytomas are rare forms of secondary hypertension, but should be considered in the differential diagnosis, regardless of age, even in very old patients.

Acute Myocardial Ischemia: Cellular Mechanisms Underlying ST Segment Elevation

PubMed Central

Di Diego, José M.; Antzelevitch, Charles

2014-01-01

The electrocardiogram (ECG) is an essential tool for the diagnosis of acute myocardial ischemia in the emergency department, as well as for that of an evolving acute myocardial infarction (AMI). Changes in the surface ECG in leads whose positive poles face the ischemic region are known to be related to injury currents flowing across the boundaries between the ischemic and the surrounding normal myocardium. Although experimental studies have also shown an endocardium to epicardium differential sensitivity to the effect of acute ischemia, the important contribution of this transmural heterogeneous response to the changes observed in the surface ECG are less appreciated by the clinical cardiologist. This review briefly discusses our current knowledge regarding the electrophysiology of the ischemic myocardium focusing primarily on the electrophysiologic changes underlying the ECG alterations observed at the onset of a transmural AMI. PMID:24742586

Abrupt opium discontinuation has no significant triggering effect on acute myocardial infarction.

PubMed

Masoomi, Mohammad; Zare, Jahangir; Nasri, Hamidreza; Mirzazadeh, Ali; Sheikhvatan, Mehrdad

2011-04-01

A deleterious effect of withdrawal symptoms due to abrupt discontinuation of opium on the cardiovascular system is one of the recent interesting topics in the cardiovascular field. The current study hypothesized that the withdrawal syndrome due to discontinuing opium might be an important trigger for the appearance of acute myocardial infarction. Eighty-one opium-addicted individuals who were candidates for cardiovascular clinical evaluation and consecutively hospitalized in the coronary care unit (CCU) ward of Shafa Hospital in Kerman between January and July 2009 were included in the study and categorized in the case group, including patients experiencing withdrawal symptoms within 6-12 h after the reduced or discontinued use of opium according to the Diagnostic and Statistical Manual of Mental Disorders-revised IV version (DSM-IV-R) criteria for opium dependence and withdrawal, and the control group, without opium withdrawal symptoms. The appearance of acute myocardial infarction was compared between the two groups using multivariable regression models. Acute myocardial infarction occurred in 50.0% of those with withdrawal symptoms and in 45.1% of patients without evidence of opium withdrawal (P = 0.669). Multivariable analysis showed that opium withdrawal symptoms were not a trigger for acute myocardial infarction adjusting for demographic characteristics, marital status, education level and common coronary artery disease risk profiles [odds ratio (OR) = 0.920, 95% confidence interval (CI) = 0.350-2.419, P = 0.866]. Also, daily dose of opium before reducing or discontinuing use did not predict the appearance of myocardial infarction in the presence of confounder variables (OR = 0.975, 95% CI = 0.832-1.143, P = 0.755). Withdrawal syndrome due to abrupt discontinuation of opium does not have a triggering role for appearance of acute myocardial infarction.

Prevalence and Prognosis of Hyperkalemia in Patients with Acute Myocardial Infarction

PubMed Central

Grodzinsky, Anna; Goyal, Abhinav; Gosch, Kensey; McCullough, Peter A.; Fonarow, Gregg C.; Mebazaa, Alexandre; Masoudi, Frederick A.; Spertus, John A.; Palmer, Biff F.; Kosiborod, Mikhail

2016-01-01

Background Hyperkalemia is common and potentially dangerous in hospitalized patients; its contemporary prevalence and prognostic importance following acute myocardial infarction are not well described. Methods In 38,689 consecutive acute myocardial infarction patients from the Cerner Health Facts database, we evaluated the association between maximum in-hospital potassium levels (max K) and in-hospital mortality. Patients were stratified by dialysis status, and grouped by max K as follows: <5 mEq/L, 5–<5.5 mEq/L, 5.5–<6.0 mEq/L, 6.0–<6.5 mEq/L, and ≥ 6.5 mEq/L. Multivariable logistic regression was used to adjust for multiple patient and site characteristics. The relationship between number of hyperkalemic values and in-hospital mortality was also evaluated. Results Of 38,689 acute myocardial infarction patients, 886 were on dialysis. The rate of hyperkalemia (max K ≥ 5.0 mEq/L) was 22.6% in non-dialysis and 66.8% in dialysis patients. Moderate-severe hyperkalemia (max K ≥ 5.5 mEq/L) occurred in 9.8% of patients. There was a steep increase in mortality with higher max K levels. In-hospital mortality exceeded 15% once max K ≥5.5 mEq/L regardless of dialysis status. The relationship between higher max K and increased mortality risk persisted after multivariable adjustment. In addition, patients with greater number of hyperkalemic values (vs. a single value) experienced higher in-hospital mortality. Conclusions Hyperkalemia is common in patients hospitalized with acute myocardial infarction. Higher max K levels and number of hyperkalemic events are associated with a steep mortality increase; with higher risks for adverse outcomes observed even at mild levels of hyperkalemia. Whether more intensive management of hyperkalemia may improve outcomes in acute myocardial infarction patients merits further study. PMID:27060233

CARD9 knockout ameliorates myocardial dysfunction associated with high fat diet-induced obesity.

PubMed

Cao, Li; Qin, Xing; Peterson, Matthew R; Haller, Samantha E; Wilson, Kayla A; Hu, Nan; Lin, Xin; Nair, Sreejayan; Ren, Jun; He, Guanglong

2016-03-01

Obesity is associated with chronic inflammation which plays a critical role in the development of cardiovascular dysfunction. Because the adaptor protein caspase recruitment domain-containing protein 9 (CARD9) in macrophages regulates innate immune responses via activation of pro-inflammatory cytokines, we hypothesize that CARD9 mediates the pro-inflammatory signaling associated with obesity en route to myocardial dysfunction. C57BL/6 wild-type (WT) and CARD9(-/-) mice were fed normal diet (ND, 12% fat) or a high fat diet (HFD, 45% fat) for 5months. At the end of 5-month HFD feeding, cardiac function was evaluated using echocardiography. Cardiomyocytes were isolated and contractile properties were measured. Immunofluorescence was performed to detect macrophage infiltration in the heart. Heart tissue homogenates, plasma, and supernatants from isolated macrophages were collected to measure the concentrations of pro-inflammatory cytokines using ELISA kits. Western immunoblotting analyses were performed on heart tissue homogenates and isolated macrophages to explore the underlying signaling mechanism(s). CARD9 knockout alleviated HFD-induced insulin resistance and glucose intolerance, prevented myocardial dysfunction with preserved cardiac fractional shortening and cardiomyocyte contractile properties. CARD9 knockout also significantly decreased the number of infiltrated macrophages in the heart with reduced myocardium-, plasma-, and macrophage-derived cytokines including IL-6, IL-1β and TNFα. Finally, CARD9 knockout abrogated the increase of p38 MAPK phosphorylation, the decrease of LC3BII/LC3BI ratio and the up-regulation of p62 expression in the heart induced by HFD feeding and restored cardiac autophagy signaling. In conclusion, CARD9 knockout ameliorates myocardial dysfunction associated with HFD-induced obesity, potentially through reduction of macrophage infiltration, suppression of p38 MAPK phosphorylation, and preservation of autophagy in the heart

C-terminal provasopressin (copeptin) as a novel and prognostic marker in acute myocardial infarction: Leicester Acute Myocardial Infarction Peptide (LAMP) study.

PubMed

Khan, Sohail Q; Dhillon, Onkar S; O'Brien, Russell J; Struck, Joachim; Quinn, Paulene A; Morgenthaler, Nils G; Squire, Iain B; Davies, Joan E; Bergmann, Andreas; Ng, Leong L

2007-04-24

The role of the vasopressin system after acute myocardial infarction is unclear. Copeptin, the C-terminal part of the vasopressin prohormone, is secreted stoichiometrically with vasopressin. We compared the prognostic value of copeptin and an established marker, N-terminal pro-B-type natriuretic peptide (NTproBNP), after acute myocardial infarction. In this prospective single-hospital study, we recruited 980 consecutive post-acute myocardial infarction patients (718 men, median [range] age 66 [24 to 95] years), with follow-up over 342 (range 0 to 764) days. Plasma copeptin was highest on admission (n=132, P<0.001, day 1 versus days 2 to 5) and reached a plateau at days 3 to 5. In the 980 patients, copeptin (measured at days 3 to 5) was elevated in patients who died (n=101) or were readmitted with heart failure (n=49) compared with survivors (median [range] 18.5 [0.6 to 441.0] versus 6.5 [0.3 to 267.0] pmol/L, P<0.0005). With logistic regression analysis, copeptin (odds ratio, 4.14, P<0.0005) and NTproBNP (odds ratio, 2.26, P<0.003) were significant independent predictors of death or heart failure at 60 days. The area under the receiver operating characteristic curves for copeptin (0.75) and NTproBNP (0.76) were similar. The logistic model with both markers yielded a larger area under the curve (0.84) than for NTproBNP (P<0.013) or copeptin (P<0.003) alone, respectively. Cox modeling predicted death or heart failure with both biomarkers (log copeptin [hazard ratio, 2.33], log NTproBNP [hazard ratio, 2.70]). In patients stratified by NTproBNP (above the median of approximately 900 pmol/L), copeptin above the median (approximately 7 pmol/L) was associated with poorer outcome (P<0.0005). Findings were similar for death and heart failure as individual end points. The vasopressin system is activated after acute myocardial infarction. Copeptin may predict adverse outcome, especially in those with an elevated NTproBNP (more than approximately 900 pmol/L).

Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice

PubMed Central

Fiechter, Danielle; Kats, Suzanne; Brands, Ruud; van Middelaar, Ben; Pasterkamp, Gerard; de Kleijn, Dominique; Seinen, Willem

2011-01-01

Background There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction. Methods Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood. Results Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group. Conclusion In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction. PMID:28357012

Differential loss of natural killer cell activity in patients with acute myocardial infarction and stable angina pectoris.

PubMed

Yan, Wenwen; Zhou, Lin; Wen, Siwan; Duan, Qianglin; Huang, Feifei; Tang, Yu; Liu, Xiaohong; Chai, Yongyan; Wang, Lemin

2015-01-01

To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls. 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells. In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both angina patients and the controls. There was no statistical difference in receptor expressions between angina patients and control group. The quantity of natural killer cells was significantly decreased in both infarction and angina patients compared with normal range (P<0.001). The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and angina patients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarction patients.

Systemic inflammatory response following acute myocardial infarction

PubMed Central

Fang, Lu; Moore, Xiao-Lei; Dart, Anthony M; Wang, Le-Min

2015-01-01

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI. PMID:26089856

Acute Heart Failure Triggered by Coronary Spasm With Transient Left Ventricular Dysfunction.

PubMed

Adachi, Yusuke; Sakakura, Kenichi; Ibe, Tatsuro; Yoshida, Nanae; Wada, Hiroshi; Fujita, Hideo; Momomura, Shin-Ichi

2017-04-06

Coronary spasm is abnormal contraction of an epicardial coronary artery resulting in myocardial ischemia. Coronary spasm induces not only depressed myocardial contractility, but also incomplete myocardial relaxation, which leads to elevated ventricular filling pressure. We herein report the case of a 55-year-old woman who had repeated acute heart failure caused by coronary spasm. Acetylcholine provocation test with simultaneous right heart catheterization was useful for the diagnosis of elevated ventricular filling pressure as well as coronary artery spasm. We should add coronary spasm to a differential diagnosis for repeated acute heart failure.

Pharmacological prevention of reperfusion injury in acute myocardial infarction. A potential role for adenosine as a therapeutic agent.

PubMed

Quintana, Miguel; Kahan, Thomas; Hjemdahl, Paul

2004-01-01

The concept of reperfusion injury, although first recognized from animal studies, is now recognized as a clinical phenomenon that may result in microvascular damage, no-reflow phenomenon, myocardial stunning, myocardial hibernation and ischemic preconditioning. The final consequence of this event is left ventricular (LV) systolic dysfunction leading to increased morbidity and mortality. The typical clinical case of reperfusion injury occurs in acute myocardial infarction (MI) with ST segment elevation in which an occlusion of a major epicardial coronary artery is followed by recanalization of the artery. This may occur either spontaneously or by means of thrombolysis and/or by primary percutaneous coronary intervention (PCI) with efficient platelet inhibition by aspirin (acetylsalicylic acid), clopidogrel and glycoprotein IIb/IIIa inhibitors. Although the pathophysiology of reperfusion injury is complex, the major role that neutrophils play in this process is well known. Neutrophils generate free radicals, degranulation products, arachidonic acid metabolites and platelet-activating factors that interact with endothelial cells, inducing endothelial injury and neutralization of nitrous oxide vasodilator capacity. Adenosine, through its multi-targeted pharmacological actions, is able to inhibit some of the above-mentioned detrimental effects. The net protective of adenosine in in vivo models of reperfusion injury is the reduction of the infarct size, the improvement of the regional myocardial blood flow and of the regional function of the ischemic area. Additionally, adenosine preserves the post-ischemic coronary flow reserve, coronary blood flow and the post-ischemic regional contractility. In small-scale studies in patients with acute MI, treatment with adenosine has been associated with smaller infarcts, less no-reflow phenomenon and improved LV function. During elective PCI adenosine reduced ST segment shifts, lactate production and ischemic symptoms. During the

Estrogen Receptors α and β Play Major Roles in Ethanol-Evoked Myocardial Oxidative Stress and Dysfunction in Conscious Ovariectomized Rats.

PubMed

Yao, Fanrong; Abdel-Rahman, Abdel A

2017-02-01

We documented the dependence of ethanol (EtOH)-evoked myocardial dysfunction on estrogen (E 2 ), and our recent estrogen receptor (ER) blockade study, in proestrus rats, implicated ERα signaling in this phenomenon. However, a limitation of selective pharmacological loss-of-function approach is the potential contribution of the other 2 ERs to the observed effects because crosstalk exists between the 3 ERs. Here, we adopted a "regain"-of-function approach (using selective ER subtype agonists) to identify the ER subtype(s) required for unraveling the E 2 -dependent myocardial oxidative stress/dysfunction caused by EtOH in conscious ovariectomized (OVX) rats. OVX rats received a selective ERα (PPT), ERβ (DPN), or GPER (G1) agonist (10 μg/kg; i.v.) or vehicle 30 minutes before EtOH (1.0 g/kg; infused i.v. over 30 minutes) or saline, and the hemodynamic recording continued for additional 60 minutes. Thereafter, left ventricular tissue was collected for conducting ex vivo molecular/biochemical studies. EtOH had no hemodynamic effects in OVX rats, but reduced the left ventricular contractility index, dP/dt max , and MAP after acute ERα (PPT) or ERβ (DPN) activation. These responses were associated with increases in the phosphorylation of ERK1/2 and eNOS, and in reactive oxygen species (ROS) and malondialdehyde (MDA) levels in the myocardium. GPER activation (G1) only unraveled a modest EtOH-evoked hypotension and elevation in myocardial ROS. PPT enhanced catalase, DPN reduced ALDH2, while G1 had no effect on the activity of either enzyme, and none of the agonists influenced alcohol dehydrogenase or CYP2E1 activities in the myocardium. Blood EtOH concentration (96.0 mg/dl) was significantly reduced following ERα (59.8 mg/dl) or ERβ (62.9 mg/dl), but not GPER (100.3 mg/dl), activation in EtOH-treated OVX rats. ERα and ERβ play major roles in the E 2 -dependent myocardial dysfunction caused by EtOH by promoting combined accumulation of cardiotoxic (ROS and

Relation of coronary flow pattern to myocardial blush grade in patients with first acute myocardial infarction

PubMed Central

Hoffmann, R; Haager, P; Lepper, W; Franke, A; Hanrath, P

2003-01-01

Background: Analysis of myocardial blush grade (MBG) and coronary flow velocity pattern has been used to obtain direct or indirect information about microvascular damage and reperfusion injury after percutaneous transluminal coronary angiography for acute myocardial infarction. Objective: To evaluate the relation between coronary blood flow velocity pattern and MBG immediately after angioplasty plus stenting for acute myocardial infarction. Design: The coronary blood flow velocity pattern in the infarct related artery was determined immediately after angioplasty in 35 patients with their first acute myocardial infarct using a Doppler guide wire. Measurements were related to MBG as a direct index of microvascular function in the infarct zone. Results: Coronary flow velocity patterns were different between patients with absent myocardial blush (n = 14), reduced blush (n = 7), or normal blush (n = 14). The following variables (mean (SD)) differed significantly between the three groups: systolic peak flow velocity (cm/s): absent blush 10.9 (4.2), reduced blush 14.2 (6.4), normal blush 19.2 (11.2); p = 0.036; diastolic deceleration rate (ms): absent blush 103 (58), reduced blush 80 (65), normal blush 50 (19); p = 0.025; and diastolic–systolic velocity ratio: absent blush 4.06 (2.18), reduced blush 2.02 (0.55), normal blush 1.88 (1.03); p = 0.002. In a multivariate analysis MBG was the only variable with a significant impact on the diastolic deceleration rate (p = 0.034,) while age, infarct location, time to revascularisation, infarct vessel diameter, and maximum creatine kinase had no significant impact. Conclusions: The coronary flow velocity pattern in the infarct related epicardial artery is primarily determined by the microvascular function of the dependent myocardium, as reflected by MBG. PMID:12975402

An unusual case of infective endocarditis presenting as acute myocardial infarction.

PubMed

Chen, Zhong; Ng, Francesca; Nageh, Thuraia

2007-06-01

A 39-year-old Zimbabwean man presented with a 1 week history of fever, general malaise and acute-onset chest pain. He had a urethral stricture, which had been managed with an indwelling supra-pubic catheter. The electrocardiography on admission showed inferior ST-T segments elevation. His chest pain and electrocardiography changes resolved subsequent to thrombolysis, and he remained haemodynamically stable. The 12-h troponin I was increased at 10.5 microg/l (NR <0.04 microg/l). Echocardiography confirmed severe mitral regurgitation and a flail anterior mitral valve leaflet with an independently oscillating mobile vegetation. Enterococci faecalis were grown on blood cultures. A diagnosis of enterococci infective endocarditis with concomitant acute myocardial infarction due to possible septic emboli was made. Despite the successful outcome from thrombolysis in the setting of acute myocardial infarction with infective endocarditis, the case highlights the current lack of definitive data on the optimal acute management of such an unusual clinical scenario. Although there is serious concern that thrombolytic treatment for myocardial infarction in the setting of infective endocarditis may be associated with higher risk of cerebral haemorrhage, there is little documented evidence supporting the safety of primary percutaneous coronary intervention with these patients.

Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both.

PubMed

Pfeffer, Marc A; McMurray, John J V; Velazquez, Eric J; Rouleau, Jean-Lucien; Køber, Lars; Maggioni, Aldo P; Solomon, Scott D; Swedberg, Karl; Van de Werf, Frans; White, Harvey; Leimberger, Jeffrey D; Henis, Marc; Edwards, Susan; Zelenkofske, Steven; Sellers, Mary Ann; Califf, Robert M

2003-11-13

Angiotensin-converting-enzyme (ACE) inhibitors such as captopril reduce mortality and cardiovascular morbidity among patients with myocardial infarction complicated by left ventricular systolic dysfunction, heart failure, or both. In a double-blind trial, we compared the effect of the angiotensin-receptor blocker valsartan, the ACE inhibitor captopril, and the combination of the two on mortality in this population of patients. Patients receiving conventional therapy were randomly assigned, 0.5 to 10 days after acute myocardial infarction, to additional therapy with valsartan (4909 patients), valsartan plus captopril (4885 patients), or captopril (4909 patients). The primary end point was death from any cause. During a median follow-up of 24.7 months, 979 patients in the valsartan group died, as did 941 patients in the valsartan-and-captopril group and 958 patients in the captopril group (hazard ratio in the valsartan group as compared with the captopril group, 1.00; 97.5 percent confidence interval, 0.90 to 1.11; P=0.98; hazard ratio in the valsartan-and-captopril group as compared with the captopril group, 0.98; 97.5 percent confidence interval, 0.89 to 1.09; P=0.73). The upper limit of the one-sided 97.5 percent confidence interval for the comparison of the valsartan group with the captopril group was within the prespecified margin for noninferiority with regard to mortality (P=0.004) and with regard to the composite end point of fatal and nonfatal cardiovascular events (P<0.001). The valsartan-and-captopril group had the most drug-related adverse events. With monotherapy, hypotension and renal dysfunction were more common in the valsartan group, and cough, rash, and taste disturbance were more common in the captopril group. Valsartan is as effective as captopril in patients who are at high risk for cardiovascular events after myocardial infarction. Combining valsartan with captopril increased the rate of adverse events without improving survival. Copyright 2003

Twenty-Five-Year (1986-2011) Trends in the Incidence and Death Rates of Stroke Complicating Acute Myocardial Infarction.

PubMed

Hariri, Essa; Tisminetzky, Mayra; Lessard, Darleen; Yarzebski, Jorge; Gore, Joel; Goldberg, Robert

2018-05-04

The occurrence of a stroke after an acute myocardial infarction is associated with increased morbidity and mortality rates. However, limited data are available, particularly from a population-based perspective, about recent trends in the incidence and mortality rates associated with stroke complicating an acute myocardial infarction. The purpose of this study was to examine 25-year trends (1986-2011) in the incidence and in-hospital mortality rates of initial episodes of stroke complicating acute myocardial infarction. The study population consisted of 11,436 adults hospitalized with acute myocardial infarction at all 11 medical centers in central Massachusetts on a biennial basis between 1986 and 2011. In this study cohort, 159 patients (1.4%) experienced an acute first-ever stroke during hospitalization for acute myocardial infarction. The proportion of patients with acute myocardial infarction who developed a stroke increased through the 1990s but decreased slightly thereafter. Compared with patients who did not experience a stroke, those who experienced a stroke were significantly older, were more likely to be female, had a previous acute myocardial infarction, had a significant burden of comorbidities, and were more likely to have died (32.1% vs 10.8%) during their index hospitalization. Patients who developed a first stroke in the most recent study years (2003-2011) were more likely to have died during hospitalization than those hospitalized during earlier study years. Although the incidence rates of acute stroke complicating acute myocardial infarction remained relatively stable during the years under study, the in-hospital mortality rates of those experiencing a stroke have not decreased. Copyright © 2018. Published by Elsevier Inc.

Estrogen receptor ERα plays a major role in ethanol-evoked myocardial oxidative stress and dysfunction in conscious female rats.

PubMed

Yao, Fanrong; Abdel-Rahman, Abdel A

2016-02-01

Our previous studies showed that ethanol elicited estrogen (E2)-dependent myocardial oxidative stress and dysfunction. In the present study we tested the hypothesis that E2 signaling via the estrogen receptor (ER), ERα, mediates this myocardial detrimental effect of alcohol. To achieve this goal, conscious female rats in proestrus phase (highest endogenous E2 level) received a selective ER antagonist (200 μg/kg; intra-venous [i.v.]) for ERα (MPP), ERβ (PHTPP) or GPER (G15) or saline 30 min before ethanol (1 g/kg; i.v.) or saline infusion. ERα blockade virtually abrogated ethanol-evoked myocardial dysfunction and hypotension, while ERβ blockade had little effect on the hypotensive response, but caused delayed attenuation of the ethanol-evoked reductions in left ventricular developed pressure and the rate of left ventricle pressure rise. GPER blockade caused delayed attenuation of all cardiovascular effects of ethanol. All three antagonists attenuated the ethanol-evoked increases in myocardial catalase and ALDH2 activities, Akt, ERK1/2, p38, eNOS, and nNOS phosphorylation, except for a lack of effect of PHTPP on p38. Finally, all three ER antagonists attenuated ethanol-evoked elevation in myocardial ROS, but this effect was most notable with ERα blockade. In conclusion, ERα plays a greater role in, and might serve as a molecular target for ameliorating, the E2-dependent myocardial oxidative stress and dysfunction caused by ethanol. Copyright © 2016 Elsevier Inc. All rights reserved.

Comparison of anxiety between smokers and nonsmokers with acute myocardial infarction.

PubMed

Sheahan, Sharon L; Rayens, Mary K; An, Kyungeh; Riegel, Barbara; McKinley, Sharon; Doering, Lynn; Garvin, Bonnie J; Moser, Debra K

2006-11-01

Increased anxiety correlates with increased complications after acute myocardial infarction. Anxiety levels and use of anxiolytic agents have not been compared between smokers and nonsmokers hospitalized because of acute myocardial infarction. To compare anxiety level, sociodemographic factors, and clinical variables between smokers and nonsmokers hospitalized with acute myocardial infarction and to examine predictors of use of beta-blockers and anxiolytic agents among smokers and nonsmokers. Secondary data analysis of a prospective multisite study on anxiety in 181 smokers and 351 nonsmokers with acute myocardial infarction. Anxiety was measured by using the State Trait Anxiety Inventory and the anxiety subscale of the Basic Symptom Inventory within 72 hours of admission. Smokers reported higher anxiety levels than nonsmokers reported on both anxiety scales. Female smokers reported the highest anxiety and peak pain levels of all, yet women were the least likely to receive anxiolytic agents. Smoking status was not a predictor for anxiety level when sex, peak pain, use of beta-blockers in the hospital, and age were controlled for. However, smokers were twice as likely as nonsmokers to receive an anxiolytic agent and 60% more likely to receive a beta-blocker in the emergency department, and smokers were 80% more likely than nonsmokers to receive an anxiolytic agent during hospitalization when these variables were controlled. Older female smokers are at risk for complications because they are older than their male counterparts and less likely to receive beta-blockers and antianxiety medications in the emergency department.

Acute myocardial infarction quality of care: the Strong Heart Study.

PubMed

Best, Lyle G; Butt, Amir; Conroy, Britt; Devereux, Richard B; Galloway, James M; Jolly, Stacey; Lee, Elisa T; Silverman, Angela; Yeh, Jeun-Liang; Welty, Thomas K; Kedan, Ilan

2011-01-01

Evaluate the quality of care provided patients with acute myocardial infarction and compare with similar national and regional data. Case series. The Strong Heart Study has extensive population-based data related to cardiovascular events among American Indians living in three rural regions of the United States. Acute myocardial infarction cases (72) occurring between 1/1/2001 and 12/31/2006 were identified from a cohort of 4549 participants. The proportion of cases that were provided standard quality of care therapy, as defined by the Healthcare Financing Administration and other national organizations. The provision of quality services, such as administration of aspirin on admission and at discharge, reperfusion therapy within 24 hours, prescription of beta blocker medication at discharge, and smoking cessation counseling were found to be 94%, 91%, 92%, 86% and 71%, respectively. The unadjusted, 30 day mortality rate was 17%. Despite considerable challenges posed by geographic isolation and small facilities, process measures of the quality of acute myocardial infarction care for participants in this American Indian cohort were comparable to that reported for Medicare beneficiaries nationally and within the resident states of this cohort.

Intravascular lymphomatosis presenting as acute hemispheric dysfunction.

PubMed

Hwang, Woo Sub; Jung, Chul Won; Ko, Young Hye; Seo, Sang Won; Na, Duk L

2012-11-01

Intravascular lymphomatosis (IVL) is known to affect both hemispheres of the brain and manifests clinically as seizures or dementia. To our knowledge, there have been no cases in which acute hemispheric dysfunction is manifested in IVL. We present a 54-year-old man who showed steroid responsive acute hemispheric dysfunction. A technetium 99m-ethyl cysteinate dimer single-photon emission computed tomographic scan of the brain revealed hypoperfusion in the right hemisphere. The bone marrow biopsy specimen confirmed malignant lymphoid cells in vessels, which suggested IVL. Our case signifies the diversity of clinical manifestations in IVL. Copyright © 2012. Published by Elsevier Inc.

[A case of rupture of the left ventricle free wall with papillary muscle dysfunction following acute myocardial infarction, operated on successfully].

PubMed

de Lima, R; Perdigão, C; Neves, L; Cravino, J; Dantas, M; Bordalo, A; Pais, F; Diogo, A N; Ferreira, R; Ribeiro, C

1990-09-01

The authors present a case of left ventricular free wall rupture post acute myocardial infarction, associated with mitral papillary posterior muscle necrosis, operated by infartectomy and mitral valvular protesis replacement. They refer the various complications occurred during the hospital staying, and discuss its medical and surgical approach. The patient was discharged alive and six months after the infarction keeps a moderate activity.

Creatine kinase radioimmunoassay and isoenzyme electrophoresis compared in the diagnosis of acute myocardial infarction

DOE Office of Scientific and Technical Information (OSTI.GOV)

Homburger, H.A.; Jacob, G.L.

1980-07-01

We compared, in 116 patients, the relative usefulness of results of tests for creatine kinase B-isoenzymes, as measured by radioimmunoassay, and the MB isoenzyme, as measured by electrophoresis, in diagnosis of acute myocardial infarction. The radioimmunoassay was specific for isoenzymes of creatine kinase containing the B subunit. All patients with acute transmural infarcts had positive test results by both techniques, but concentrations of B-isoenzymes were more frequently above normal than were MB bands in the case of patients with acute subendocardial infarcts and in the case of all patients with acute myocardial infarcts from whom sera were collected more thanmore » 24 h after onset of chest pain. Concentrations of B-isoenzymes also were increased, even when MB bands were not electrophoretically detectable in specimens from several patients without documented acute myocardial infarcts. These abnormal results presumably were caused by increased concentrations of the BB isoenzyme in serum. Accordingly, an increased concentration of B-isoenzymes had less diagnostic specificity and predictive value for acute myocardial infarction than did a detectable MB band. Results of isoenzyme electrophoresis were more reliable for establishing this diagnosis, but the results of radioimmunoassay were more reliable for excluding it in patients with chest pain as the primary symptom.« less

N-terminal pro B-type natriuretic peptide in the early evaluation of suspected acute myocardial infarction.

PubMed

Haaf, Philip; Balmelli, Cathrin; Reichlin, Tobias; Twerenbold, Raphael; Reiter, Miriam; Meissner, Julia; Schaub, Nora; Stelzig, Claudia; Freese, Michael; Paniz, Patricia; Meune, Christophe; Drexler, Beatrice; Freidank, Heike; Winkler, Katrin; Hochholzer, Willibald; Mueller, Christian

2011-08-01

Myocardial ischemia is a strong trigger of N-terminal pro-B-type natriuretic peptide (NT-proBNP) release. As ischemia precedes necrosis in acute myocardial infarction, we hypothesized that NT-proBNP might be useful in the early diagnosis and risk stratification of patients with suspected acute myocardial infarction. In a prospective multicenter study, NT-proBNP was measured at presentation in 658 consecutive patients with acute chest pain. The final diagnosis was adjudicated by 2 independent cardiologists. Patients were followed long term regarding mortality. Acute myocardial infarction was the adjudicated final diagnosis in 117 patients (18%). NT-proBNP levels at presentation were significantly higher in acute myocardial infarction as compared with patients with other final diagnoses (median 886 pg/mL vs 135 pg/mL, P <.001). The diagnostic accuracy of NT-proBNP for acute myocardial infarction as quantified by the area under the receiver operating characteristic curve (AUC) was 0.79 (95% confidence interval [CI], 0.75-0.83). When added to cardiac troponin T, NT-proBNP significantly increased the AUC from 0.89 (95% CI, 0.84-0.93) to 0.91 (95% CI, 0.88-0.94; P=.033). Cumulative 24-month mortality rates were 0% in the first, 1.3% in the second, 8.3% in the third, and 23.3% in the fourth quartile of NT-proBNP (P <.001). NT-proBNP (AUC 0.85, 95% CI, 0.81-0.89) predicted all-cause mortality independently of and more accurately than both cardiac troponin T (AUC 0.66, 95% CI, 0.58-0.74; P <.001) and the Thrombolysis in Myocardial Infarction risk score (AUC 0.79, 95% CI, 0.74-0.84; P <.001). Net reclassification improvement (Thrombolysis in Myocardial Infarction vs additionally NT-proBNP) was 0.188 (P <.009), and integrated discrimination improvement was 0.100 (P <.001). Use of NT-proBNP improves the early diagnosis and risk stratification of patients with suspected acute myocardial infarction. Copyright © 2011 Elsevier Inc. All rights reserved.

Early detection of myocardial dysfunction using two-dimensional speckle tracking echocardiography in a young cat with hypertrophic cardiomyopathy

PubMed Central

Mochizuki, Yohei; Yoshimatsu, Hiroki; Niina, Ayaka; Teshima, Takahiro; Matsumoto, Hirotaka; Koyama, Hidekazu

2018-01-01

Case summary A 5-month-old intact female Scottish Fold cat was presented for cardiac evaluation. Careful auscultation detected a slight systolic murmur (Levine I/VI). The findings of electrocardiography, thoracic radiography, non-invasive blood pressure measurements and conventional echocardiographic studies were unremarkable. However, two-dimensional speckle tracking echocardiography revealed abnormalities in myocardial deformations, including decreased early-to-late diastolic strain rate ratios in longitudinal, radial and circumferential directions, and deteriorated segmental systolic longitudinal strain. At the follow-up examinations, the cat exhibited echocardiographic left ventricular hypertrophy and was diagnosed with hypertrophic cardiomyopathy using conventional echocardiography. Relevance and novel information This is the first report on the use of two-dimensional speckle tracking echocardiography for the early detection of myocardial dysfunction in a cat with hypertrophic cardiomyopathy; the myocardial dysfunction was detected before the development of hypertrophy. The findings from this case suggest that two-dimensional speckle tracking echocardiography can be useful for myocardial assessment when conventional echocardiographic and Doppler findings are ambiguous. PMID:29449957

Prevalence and Prognosis of Hyperkalemia in Patients with Acute Myocardial Infarction.

PubMed

Grodzinsky, Anna; Goyal, Abhinav; Gosch, Kensey; McCullough, Peter A; Fonarow, Gregg C; Mebazaa, Alexandre; Masoudi, Frederick A; Spertus, John A; Palmer, Biff F; Kosiborod, Mikhail

2016-08-01

Hyperkalemia is common and potentially dangerous in hospitalized patients; its contemporary prevalence and prognostic importance after acute myocardial infarction are not well described. In 38,689 consecutive patients with acute myocardial infarction from the Cerner Health Facts database, we evaluated the association between maximum in-hospital potassium levels and in-hospital mortality. Patients were stratified by dialysis status and grouped by maximum potassium as follows: <5 mEq/L, 5 to <5.5 mEq/L, 5.5 to <6.0 mEq/L, 6.0 to <6.5 mEq/L, and ≥6.5 mEq/L. Multivariable logistic regression was used to adjust for multiple patient and site characteristics. The relationship between the number of hyperkalemic values and the in-hospital mortality was evaluated. Of 38,689 patients with acute myocardial infarction, 886 were on dialysis. The rate of hyperkalemia (maximum potassium ≥5.0 mEq/L) was 22.6% in patients on dialysis and 66.8% in patients not on dialysis. Moderate to severe hyperkalemia (maximum potassium ≥5.5 mEq/L) occurred in 9.8% of patients. There was a steep increase in mortality with higher maximum potassium levels. In-hospital mortality exceeded 15% once maximum potassium was ≥5.5 mEq/L regardless of dialysis status. The relationship between higher maximum potassium and increased mortality risk persisted after multivariable adjustment. In addition, patients with a greater number of hyperkalemic values (vs a single value) experienced higher in-hospital mortality. Hyperkalemia is common in patients who are hospitalized with acute myocardial infarction. Higher maximum potassium levels and number of hyperkalemic events are associated with a steep mortality increase, with higher risks for adverse outcomes observed even at mild levels of hyperkalemia. Whether more intensive management of hyperkalemia may improve outcomes in patients with acute myocardial infarction merits further study. Copyright © 2016 Elsevier Inc. All rights reserved.

Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

DOE Office of Scientific and Technical Information (OSTI.GOV)

Watanabe, Tomoyuki; Saotome, Masao, E-mail: msaotome@hama-med.ac.jp; Nobuhara, Mamoru

Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ{sub m}) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H{sub 2}O{sub 2}),more » they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ{sub m} depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H{sub 2}O{sub 2}-induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ{sub m} depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin

Nitroglycerin Use in Myocardial Infarction Patients: Risks and Benefits

PubMed Central

Ferreira, Julio C.B.; Mochly-Rosen, Daria

2012-01-01

Acute myocardial infarction and its sequelae are leading causes of morbidity and mortality worldwide. Nitroglycerin remains a first-line treatment for angina pectoris and acute myocardial infarction. Nitroglycerin achieves its benefit by giving rise to nitric oxide, which causes vasodilation and increases blood flow to the myocardium. However, continuous delivery of nitroglycerin results in tolerance, limiting the use of this drug. Nitroglycerin tolerance is due, at least in part, to inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts nitroglycerin to the vasodilator, nitric oxide. We have recently found that, in addition to nitroglycerin’s effect on the vasculature, sustained treatment with nitroglycerin negatively affects cardiomyocyte viability following ischemia, thus resulting in increased infarct size in a myocardial infarction model in animals. Co-administration of Alda-1, an activator of ALDH2, with nitroglycerin improves metabolism of reactive aldehyde adducts and prevents the nitroglycerin-induced increase in cardiac dysfunction following myocardial infarction. In this review, we describe the molecular mechanisms associated with the benefits and risks of nitroglycerin administration in myocardial infarction. (167 of 200). PMID:22040938

Thrombus aspiration in acute myocardial infarction: concepts, clinical trials, and current guidelines.

PubMed

Vandermolen, Sebastian; Marciniak, Maciej; Byrne, Jonathan; De Silva, Kalpa

2016-05-01

The pathogenesis that underlies acute myocardial infarction is complex and multifactorial. One of the most important components, however, is the role of thrombus formation following atherosclerotic plaque rupture, leading to sudden coronary occlusion and subsequent ischemia and infarction. Thrombus aspiration provides the opportunity of intracoronary clot extraction with the aim to improve coronary and myocardial perfusion, by reducing the risk of no-reflow secondary to distal embolization of thrombus. The utility of thrombus aspiration during primary percutaneous coronary intervention has been assessed in an increasing number of observational and randomized studies. This article reviews the contemporary data and provides insights into the validity of thrombus aspiration in the setting of acute myocardial infarction.

[Myocardial imaging in acute myocardial infarction using beta-methyl-p-(123I)-iodophenylpentadecanoic acid: comparison with 201Tl imaging and wall motion].

PubMed

Naruse, H; Itano, M; Kondo, T; Kogame, T; Yamamoto, J; Morita, M; Kawamoto, H; Fukutake, N; Ohyanagi, M; Iwasaki, T

1992-01-01

Myocardial imaging using beta-methyl-p-(123I)-iodophenylpentadecanoic acid (BMIPP) was performed in 11 patients with acute myocardial infarction. The left ventricular images were divided into 12 segments, and myocardial imagings with BMIPP were compared with coronary angiography (CAG), thallium-201 myocardial scintigraphy (TL) and wall motion obtained by two-dimensional echocardiography (WM). When the culprit lesion was at the proximal point of the left anterior descending artery (LAD), all segments showed depressed uptake. In 3 cases with single vessel disease of the LAD, inferior wall of the basis showed reduced uptake of BMIPP despite the location of the culprit lesion. In cases with discordant uptake between the two tracers, BMIPP frequently showed more severely depressed uptake than TL in the subacute phase, although the uptake of BMIPP correlated with that of TL (tau = 0.82, p less than 0.001). In such cases, the discordance was related to the improvement in WM from the acute phase to the convalescent phase. BMIPP uptake correlated with WM in the subacute phase (tau = 0.50, p less than 0.001). BMIPP showed more severely depressed uptake while WM showed mild asynergy in most cases in which discordance was found between the BMIPP and WM findings. However, there was no correlation between the change in WM from the acute to subacute phases, or the uptakes of BMIPP and TL alone. We concluded that the myocardial condition can be evaluated in detail in acute myocardial infarction by comparing the findings of BMIPP with those of TL and WM.

Differences in the Korea Acute Myocardial Infarction Registry Compared with Western Registries

PubMed Central

2017-01-01

The Korea Acute Myocardial Infarction Registry (KAMIR) is the first nationwide registry that reflects current therapeutic approaches and acute myocardial infarction (AMI) management in Korea. The results of the KAMIR demonstrated different risk factors and responses to medical and interventional treatments. The results indicated that the incidence of ST-elevation myocardial infarction (STEMI) was relatively high, and that the prevalence of dyslipidemia was relatively low with higher triglyceride and lower high-density lipoprotein cholesterol levels. Percutaneous coronary intervention (PCI) rates were high for both STEMI and non-ST-elevation myocardial infarction (NSTEMI) with higher use of drug-eluting stents (DESs). DES were effective and safe without increased risk of stent thrombosis in Korean AMI patients. Triple antiplatelet therapy, consisting of aspirin, clopidogrel, and cilostazol, was effective in preventing adverse clinical outcomes after PCI. Statin therapy was effective in Korean AMI patients, including those with very low levels of low-density lipoprotein cholesterol and those with cardiogenic shock. The KAMIR score had a greater predictive value than Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) scores for long-term mortality in AMI patients. Based on these results, the KAMIR will be instrumental for establishing new therapeutic strategies and effective methods for secondary prevention of AMI and guidelines for Asian patients. PMID:29035427

Cardioprotective effects of gallic acid in diabetes-induced myocardial dysfunction in rats

PubMed Central

Patel, Snehal S.; Goyal, Ramesh K.

2011-01-01

Background: Normalization of hyperglycemia, hyperlipidemia, and oxidative stress is an important objective in preventing diabetes-induced cardiac dysfunction. Objective: This study was undertaken to examine the effects of gallic acid in myocardial dysfunctions associated with type-1 diabetes. Materials and Methods: Diabetes was induced by single intravenous injection of streptozotocin (STZ, 50 mg/kg i.v.). Gallic acid was administered daily at three different doses (100, 50, and 25 mg/kg p.o.) for 8 weeks at the end of which blood samples were collected and analyzed for various biochemical parameters. Results: Injection of STZ produced significant loss of body weight (BW), polyphagia, polydypsia, hyperglycemia, hypoinsulinemia, hyperlipidemia, hypertension, bradycardia, and myocardial functional alterations. Treatment with gallic acid significantly lowered fasting glucose, the AUCglucose level in a dose-dependent manner; however, the insulin level was not increased significantly at same the dose and prevented loss of BW, polyphagia, and polydypsia in diabetic rats. It also prevented STZ-induced hyperlipidemia, hypertension, bradycardia, structural alterations in cardiac tissue such as increase in force of contraction, left ventricular weight to body weight ratio, collagen content, protein content, serum lactate dehydrogenase, and creatinine kinase levels in a dose-dependent manner. Further, treatment also produced reduction in lipid peroxidation and increase in antioxidant parameters in heart of diabetic rats. Conclusion: The results of this study suggest that gallic acid to be beneficial for the treatment of myocardial damage associated with type-1 diabetes. PMID:22224046

Local sympathetic denervation attenuates myocardial inflammation and improves cardiac function after myocardial infarction in mice

PubMed Central

Ziegler, Karin A; Ahles, Andrea; Wille, Timo; Kerler, Julia; Ramanujam, Deepak; Engelhardt, Stefan

2018-01-01

Abstract Aims Cardiac inflammation has been suggested to be regulated by the sympathetic nervous system (SNS). However, due to the lack of methodology to surgically eliminate the myocardial SNS in mice, neuronal control of cardiac inflammation remains ill-defined. Here, we report a procedure for local cardiac sympathetic denervation in mice and tested its effect in a mouse model of heart failure post-myocardial infarction. Methods and results Upon preparation of the carotid bifurcation, the right and the left superior cervical ganglia were localized and their pre- and postganglionic branches dissected before removal of the ganglion. Ganglionectomy led to an almost entire loss of myocardial sympathetic innervation in the left ventricular anterior wall. When applied at the time of myocardial infarction (MI), cardiac sympathetic denervation did not affect acute myocardial damage and infarct size. In contrast, cardiac sympathetic denervation significantly attenuated chronic consequences of MI, including myocardial inflammation, myocyte hypertrophy, and overall cardiac dysfunction. Conclusion These data suggest a critical role for local sympathetic control of cardiac inflammation. Our model of myocardial sympathetic denervation in mice should prove useful to further dissect the molecular mechanisms underlying cardiac neural control. PMID:29186414

Cardiac DPP-4 inhibition by saxagliptin ameliorates isoproterenol-induced myocardial remodeling and cardiac diastolic dysfunction in rats.

PubMed

Ikeda, Junichi; Kimoto, Naoya; Kitayama, Tetsuya; Kunori, Shunji

2016-09-01

Saxagliptin, a potent and selective DPP-4 inhibitor, is characterized by its slow dissociation from DPP-4 and its long half-life and is expected to have a potent tissue membrane-bound DPP-4-inhibitory effect in various tissues. In the present study, we examined the effects of saxagliptin on in situ cardiac DPP-4 activity. We also examined the effects of saxagliptin on isoproterenol-induced the changes in the early stage such as, myocardial remodeling and cardiac diastolic dysfunction. Male SD rats treated with isoproterenol (1 mg/kg/day via osmotic pump) received vehicle or saxagliptin (17.5 mg/kg via drinking water) for 2 weeks. In situ cardiac DPP-4 activity was measured by a colorimetric assay. Cardiac gene expressions were examined and an echocardiographic analysis was performed. Saxagliptin treatment significantly inhibited in situ cardiac DPP-4 activity and suppressed isoproterenol-induced myocardial remodeling and the expression of related genes without altering the blood glucose levels. Saxagliptin also significantly ameliorated cardiac diastolic dysfunction in isoproterenol-treated rats. In conclusion, the inhibition of DPP-4 activity in cardiac tissue by saxagliptin was associated with suppression of myocardial remodeling and cardiac diastolic dysfunction independently of its glucose-lowering action in isoproterenol-treated rats. Cardiac DPP-4 activity may contribute to myocardial remodeling in the development of heart failure. Copyright © 2016 Kyowa Hakko Kirin Co.,Ltd. Production and hosting by Elsevier B.V. All rights reserved.

Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

El-Mas, Mahmoud M., E-mail: mahelm@hotmail.com; Abdel-Rahman, Abdel A., E-mail: abdelrahmana@ecu.edu

Evidence suggests that male rats are protected against the hypotensive and myocardial depressant effects of ethanol compared with females. We investigated whether E{sub 2} modifies the myocardial and oxidative effects of ethanol in male rats. Conscious male rats received ethanol (0.5, 1 or 1.5 g/kg i.v.) 30-min after E{sub 2} (1 μg/kg i.v.) or its vehicle (saline), and hearts were collected at the conclusion of hemodynamic measurements for ex vivo molecular studies. Ethanol had no effect in vehicle-treated rats, but it caused dose-related reductions in LV developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of rise in LV pressure (dP/dt{sub max})more » and systolic (SBP) and diastolic (DBP) blood pressures in E{sub 2}-pretreated rats. These effects were associated with elevated (i) indices of reactive oxygen species (ROS), (ii) malondialdehyde (MDA) protein adducts, and (iii) phosphorylated death-associated protein kinase-3 (DAPK3), Akt, and extracellular signal-regulated kinases (ERK1/2). Enhanced myocardial anti-oxidant enzymes (heme oxygenase-1, catalase and aldehyde dehydrogenase 2) activities were also demonstrated. In conclusion, E{sub 2} promotes ethanol-evoked myocardial oxidative stress and dysfunction in male rats. The present findings highlight the risk of developing myocardial dysfunction in men who consume alcohol while receiving E{sub 2} for specific medical conditions. - Highlights: • Ethanol lowers blood pressure and causes LV dysfunction in E{sub 2}-treated rats. • E{sub 2}/ethanol aggravates cardiac oxidative state via of DAPK3/Akt/ERK activation. • E{sub 2}/ethanol causes a feedback increase in cardiac HO-1, catalase and ALDH2. • Alcohol might increase risk of myocardial dysfunction in men treated with E{sub 2}.« less

Acute ST-Elevation Myocardial Infarction, a Unique Complication of Recreational Nitrous Oxide Use.

PubMed

Indraratna, Praveen; Alexopoulos, Chris; Celermajer, David; Alford, Kevin

2017-08-01

A 28-year-old male was admitted to hospital with an acute ST-elevation myocardial infarction. This was in the context of recreational abuse of nitrous oxide. The prevalence of nitrous oxide use in Australia has not been formally quantified, however it is the second most commonly used recreational drug in the United Kingdom. Nitrous oxide has previously been shown to increase serum homocysteine levels. This patient was discovered to have an elevated homocysteine level at baseline, which was further increased after nitrous oxide consumption. Homocysteine has been linked to endothelial dysfunction and coronary atherosclerosis and this case report highlights one of the dangers of recreational abuse of nitrous oxide. Copyright © 2017 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.

Elevated troponin I levels in acute liver failure: is myocardial injury an integral part of acute liver failure?

PubMed

Parekh, Nimisha K; Hynan, Linda S; De Lemos, James; Lee, William M

2007-06-01

Although rare instances of cardiac injury or arrhythmias have been reported in acute liver failure (ALF), overall, the heart is considered to be spared in this condition. Troponin I, a sensitive and specific marker of myocardial injury, may be elevated in patients with sepsis and acute stroke without underlying acute coronary syndrome, indicating unrecognized cardiac injury in these settings. We sought to determine whether subclinical cardiac injury might also occur in acute liver failure. Serum troponin I levels were measured in 187 patients enrolled in the US Acute Liver Failure Study Group registry, and correlated with clinical variables and outcomes. Diagnoses were representative of the larger group of >1000 patients thus far enrolled and included 80 with acetaminophen-related injury, 26 with viral hepatitis, 19 with ischemic injury, and 62 others. Overall, 74% of patients had elevated troponin I levels (>0.1 ng/ml). Patients with elevated troponin I levels were more likely to have advanced hepatic coma (grades III or IV) or to die (for troponin I levels >0.1 ng/ml, odds ratio 3.88 and 4.69 for advanced coma or death, respectively). In acute liver failure, subclinical myocardial injury appears to occur more commonly than has been recognized, and its pathogenesis in the context of acute liver failure is unclear. Elevated troponin levels are associated with a significant increase in morbidity and mortality. Measurement of troponin I levels may be helpful in patients with acute liver failure, to detect unrecognized myocardial damage and as a marker of unfavorable outcome.

The role of technetium-99m stannous pyrophosphate in myocardial imaging to recognize, localize and identify extension of acute myocardial infarction in patients

NASA Technical Reports Server (NTRS)

Willerson, J. T.; Parkey, R. W.; Bonte, F. J.; Stokely, E. M.; Buja, E. M.

1975-01-01

The ability of technetium-99m stannous pyrophosphate myocardial scintigrams to aid diagnostically in recognizing, localizing, and identifying extension of acute myocardial infarction in patients was evaluated. The present study is an extension of previous animal and patient evaluations that were recently performed utilizing this myocardial imaging agent.

Direct T2 Quantification of Myocardial Edema in Acute Ischemic Injury

PubMed Central

Verhaert, David; Thavendiranathan, Paaladinesh; Giri, Shivraman; Mihai, Georgeta; Rajagopalan, Sanjay; Simonetti, Orlando P.; Raman, Subha V.

2014-01-01

OBJECTIVES To evaluate the utility of rapid, quantitative T2 mapping compared with conventional T2-weighted imaging in patients presenting with various forms of acute myocardial infarction. BACKGROUND T2-weighted cardiac magnetic resonance (CMR) identifies myocardial edema before the onset of irreversible ischemic injury and has shown value in risk-stratifying patients with chest pain. Clinical acceptance of T2-weighted CMR has, however, been limited by well-known technical problems associated with existing techniques. T2 quantification has recently been shown to overcome these problems; we hypothesized that T2 measurement in infarcted myocardium versus remote regions versus zones of microvascular obstruction in acute myocardial infarction patients could help reduce uncertainty in interpretation of T2-weighted images. METHODS T2 values using a novel mapping technique were prospectively recorded in 16 myocardial segments in 27 patients admitted with acute myocardial infarction. Regional T2 values were averaged in the infarct zone and remote myocardium, both defined by a reviewer blinded to the results of T2 mapping. Myocardial T2 was also measured in a group of 21 healthy volunteers. RESULTS T2 of the infarct zone was 69 ± 6 ms compared with 56 ± 3.4 ms for remote myocardium (p < 0.0001). No difference in T2 was observed between remote myocardium and myocardium of healthy volunteers (56 ± 3.4 ms and 55.5 ± 2.3 ms, respectively, p = NS). T2 mapping allowed for the detection of edematous myocardium in 26 of 27 patients; by comparison, segmented breath-hold T2-weighted short tau inversion recovery images were negative in 7 and uninterpretable in another 2 due to breathing artifacts. Within the infarct zone, areas of microvascular obstruction were characterized by a lower T2 value (59 ± 6 ms) compared with areas with no microvascular obstruction (71.6 ± 10 ms, p < 0.0001). T2 mapping provided consistent high-quality results in patients unable to breath-hold and in

Educational Level and Long-term Mortality in Patients With Acute Myocardial Infarction.

PubMed

Consuegra-Sánchez, Luciano; Melgarejo-Moreno, Antonio; Galcerá-Tomás, José; Alonso-Fernández, Nuria; Díaz-Pastor, Ángela; Escudero-García, Germán; Jaulent-Huertas, Leticia; Vicente-Gilabert, Marta

2015-11-01

The value of socioeconomic status as a prognostic marker in acute myocardial infarction is controversial. The aim of this study was to evaluate the impact of educational level, as a marker of socioeconomic status, on the prognosis of long-term survival after acute myocardial infarction. We conducted a prospective, observational study of 5797 patients admitted to hospital with acute myocardial infarction. We studied long-term all-cause mortality (median 8.5 years) using adjusted regression models. We found that 73.1% of patients had primary school education (n=4240), 14.5% had secondary school education (including high school) (n=843), 7.0% was illiterate (n=407), and 5.3% had higher education (n=307). Patients with secondary school or higher education were significantly younger, more were male, and they had fewer risk factors and comorbidity. These patients arrived sooner at hospital and had less severe heart failure. During admission they received more reperfusion therapy and their crude mortality was lower. Their drug treatment in hospital and at discharge followed guideline recommendations more closely. On multivariate analysis, secondary school or higher education was an independent predictor and protective factor for long-term mortality (hazard ratio=0.85; 95% confidence interval, 0.74-0.98). Our study shows an inverse and independent relationship between educational level and long-term mortality in patients with acute myocardial infarction. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

[Acute myocardial infarction with ST-segment elevation: Code I].

PubMed

Borrayo-Sánchez, Gabriela; Rosas-Peralta, Martín; Pérez-Rodríguez, Gilberto; Ramírez-Árias, Erick; Almeida-Gutiérrez, Eduardo; Arriaga-Dávila, José de Jesús

2018-01-01

Code infarction is a timely strategy for the treatment of acute myocardial infarction (AMI) with elevation of the ST segment. This strategy has shown an increase in survival and quality of life of patients suffering from this event around the world. The processes of management and disposition aimed at the reduction of time for effective and timely reperfusion are undoubtedly a continuous challenge. In the Instituto Mexicano del Seguro Social (IMSS) the mortality due to AMI has been reduced more than 50%, which is a historical situation that deserves much attention. Nonetheless, the continuous improvement and a wider coverage of this strategy in our country are the key factors that will outline a change in the natural history of the leading cause of death in Mexico. This review focuses on current strategies for the management of patients with acute myocardial infarction.

Myocardial Bridge and Acute Plaque Rupture

PubMed Central

Perl, Leor; Daniels, David; Schwartz, Jonathan; Tanaka, Shige; Yeung, Alan; Tremmel, Jennifer A.; Schnittger, Ingela

2016-01-01

A myocardial bridge (MB) is a common anatomic variant, most frequently located in the left anterior descending coronary artery, where a portion of the coronary artery is covered by myocardium. Importantly, MBs are known to result in a proximal atherosclerotic lesion. It has recently been postulated that these lesions predispose patients to acute coronary events, even in cases of otherwise low-risk patients. One such mechanism may involve acute plaque rupture. In this article, we report 2 cases of patients with MBs who presented with acute coronary syndromes despite having low cardiovascular risk. Their presentation was life-risking and both were treated urgently and studied with coronary angiographies and intravascular ultrasound. This latter modality confirmed a rupture of an atherosclerotic plaque proximal to the MB as a likely cause of the acute events. These cases, of unexplained acute coronary syndrome in low-risk patients, raise the question of alternative processes leading to the event and the role MB play as an underlying cause of ruptured plaques. In some cases, an active investigation for this entity may be warranted, due to the prognostic implications of the different therapeutic modalities, should an MB be discovered. PMID:28251167

Myocardial Bridge and Acute Plaque Rupture.

PubMed

Perl, Leor; Daniels, David; Schwartz, Jonathan; Tanaka, Shige; Yeung, Alan; Tremmel, Jennifer A; Schnittger, Ingela

2016-01-01

A myocardial bridge (MB) is a common anatomic variant, most frequently located in the left anterior descending coronary artery, where a portion of the coronary artery is covered by myocardium. Importantly, MBs are known to result in a proximal atherosclerotic lesion. It has recently been postulated that these lesions predispose patients to acute coronary events, even in cases of otherwise low-risk patients. One such mechanism may involve acute plaque rupture. In this article, we report 2 cases of patients with MBs who presented with acute coronary syndromes despite having low cardiovascular risk. Their presentation was life-risking and both were treated urgently and studied with coronary angiographies and intravascular ultrasound. This latter modality confirmed a rupture of an atherosclerotic plaque proximal to the MB as a likely cause of the acute events. These cases, of unexplained acute coronary syndrome in low-risk patients, raise the question of alternative processes leading to the event and the role MB play as an underlying cause of ruptured plaques. In some cases, an active investigation for this entity may be warranted, due to the prognostic implications of the different therapeutic modalities, should an MB be discovered.

Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association.

PubMed

Mehta, Laxmi S; Beckie, Theresa M; DeVon, Holli A; Grines, Cindy L; Krumholz, Harlan M; Johnson, Michelle N; Lindley, Kathryn J; Vaccarino, Viola; Wang, Tracy Y; Watson, Karol E; Wenger, Nanette K

2016-03-01

Cardiovascular disease is the leading cause of mortality in American women. Since 1984, the annual cardiovascular disease mortality rate has remained greater for women than men; however, over the last decade, there have been marked reductions in cardiovascular disease mortality in women. The dramatic decline in mortality rates for women is attributed partly to an increase in awareness, a greater focus on women and cardiovascular disease risk, and the increased application of evidence-based treatments for established coronary heart disease. This is the first scientific statement from the American Heart Association on acute myocardial infarction in women. Sex-specific differences exist in the presentation, pathophysiological mechanisms, and outcomes in patients with acute myocardial infarction. This statement provides a comprehensive review of the current evidence of the clinical presentation, pathophysiology, treatment, and outcomes of women with acute myocardial infarction. © 2016 American Heart Association, Inc.

[Use of antihypoxants in the acute period of myocardial infarction].

PubMed

Semigolovskiĭ, N Iu

1998-01-01

A total of 620 patients with acute myocardial infarction were followed up in order to assess the efficacy of antihypoxants as a component of intensive care. 385 of these patients, divided into groups of 20-40 subjects, were administered one of 12 antihypoxants or sessions of hyperbaric oxygenation during the acute period of the disease, the rest were treated traditionally. Analysis of clinical, laboratory, and prognostic values showed the highest protective effect of amtizol, lithium hydroxybutyrate, piracetam, and ubiquinone. Cytochrome C, riboxine, mildronate, and olifen were somewhat less active, and solcoseryl, bemitil, trimethasidine, and aspisol were the least effective. The protective potentialities of standard sessions of hyperbaric oxygenation were virtually null. The author proposes a parameter D, reflecting the difference between actual and predicted mortality, and the rating (score) system for assessing the routine laboratory diagnostic tests to be used together with the known criteria for evaluation of the protective effects of antihypoxants in patients with acute myocardial infarction.

Cardiac magnetic resonance imaging parameters as surrogate endpoints in clinical trials of acute myocardial infarction

PubMed Central

2011-01-01

Cardiac magnetic resonance (CMR) offers a variety of parameters potentially suited as surrogate endpoints in clinical trials of acute myocardial infarction such as infarct size, myocardial salvage, microvascular obstruction or left ventricular volumes and ejection fraction. The present article reviews each of these parameters with regard to the pathophysiological basis, practical aspects, validity, reliability and its relative value (strengths and limitations) as compared to competitive modalities. Randomized controlled trials of acute myocardial infarction which have used CMR parameters as a primary endpoint are presented. PMID:21917147

Emotions delay care-seeking in patients with an acute myocardial infarction.

PubMed

Nymark, Carolin; Mattiasson, Anne-Cathrine; Henriksson, Peter; Kiessling, Anna

2014-02-01

In acute myocardial infarction the risk of death and loss of myocardial tissue is at its highest during the first few hours. However, the process from symptom onset to the decision to seek medical care can take time. To comprehend patients' pre-hospital delay, attention must be focused on the circumstances preceding the decision to seek medical care. To add a deeper understanding of patients' thoughts, feelings and actions that preceded the decision to seek medical care when afflicted by an acute myocardial infarction. Fourteen men and women with a first or second acute myocardial infarction were interviewed individually in semi-structured interviews. Data were analysed by qualitative content analysis. Four themes were conceptualized: 'being incapacitated by fear, anguish and powerlessness', 'being ashamed of oneself', 'fear of losing a healthy identity' and 'striving to avoid fear by not interacting with others'. Patients were torn between feelings such as anguish, fear, shame and powerlessness. They made an effort to uphold their self-image as being a healthy person thus affected by an unrecognized discomfort. This combined with a struggle to protect others from involvement, strengthened the barriers to seeking care. The present study indicates that emotional reactions are important and influence patients' pre-hospital behaviour. Being ashamed of oneself stood out as a novel finding. Emotions might be an important explanation of undesired and persisting patient delays. However, our findings have to and should be evaluated quantitatively. Such a study is in progress.

Rapid Rule-Out of Acute Myocardial Injury Using a Single High-Sensitivity Cardiac Troponin I Measurement.

PubMed

Sandoval, Yader; Smith, Stephen W; Shah, Anoop S V; Anand, Atul; Chapman, Andrew R; Love, Sara A; Schulz, Karen; Cao, Jing; Mills, Nicholas L; Apple, Fred S

2017-01-01

Rapid rule-out strategies using high-sensitivity cardiac troponin assays are largely supported by studies performed outside the US in selected cohorts of patients with chest pain that are atypical of US practice, and focused exclusively on ruling out acute myocardial infarction (AMI), rather than acute myocardial injury, which is more common and associated with a poor prognosis. Prospective, observational study of consecutive patients presenting to emergency departments [derivation (n = 1647) and validation (n = 2198) cohorts], where high-sensitivity cardiac troponin I (hs-cTnI) was measured on clinical indication. The negative predictive value (NPV) and diagnostic sensitivity of an hs-cTnI concentration acute myocardial injury and for AMI or cardiac death at 30 days. In patients with hs-cTnI concentrations <99th percentile at presentation, acute myocardial injury occurred in 8.3% and 11.0% in the derivation and validation cohorts, respectively. In the derivation cohort, 27% had hs-cTnI < LoD, with NPV and diagnostic sensitivity for acute myocardial injury of 99.1% (95% CI, 97.7-99.8) and 99.0% (97.5-99.7) and an NPV for AMI or cardiac death at 30 days of 99.6% (98.4-100). In the validation cohort, 22% had hs-cTnI acute myocardial injury of 98.8% (97.9-99.7) and 99.3% (98.7-99.8) and an NPV for AMI or cardiac death at 30 days of 99.1% (98.2-99.8). A single hs-cTnI concentration acute myocardial injury, regardless of etiology, with an excellent NPV and diagnostic sensitivity, and identifies patients at minimal risk of AMI or cardiac death at 30 days. ClinicalTrials.gov Identifier: NCT02060760. © 2016 American Association for Clinical Chemistry.

[Effect of puerarin in myocardial protection in rats with acute and chronic alcoholism].

PubMed

Cui, Shu-qin

2011-12-01

To investigate the protective effect of puerarin on the myocardium of rats with acute and chronic alcoholism. In acute alcoholism experiment, normal male SD rats were randomly divided into the control group, alcoholism group and puerarin group (n=8), and high- and low-dose puerarin was administered. In chronic alcoholism experiment, increasing puerarin doses were given. Serum and myocardial levels of spartate aminotransferase (AST) and creatine phosphokinase (CPK) were determined using enzymatic methed, and superoxide dismutase (SOD), malondialdehyde (MDA), Ca(2+)-Mg(2+)-ATPase, and Na(+)-K(+)-ATPase in the myocardium were assayed with colorimetric method. HE staining was used to observe the microscopic changes of the myocardium. Compared with alcoholism group, puerarin-treated groups showed significantly lowered myocardial contents of MDA, CPK and AST and serum levels of AST and CPK (P<0.05, P<0.01) and increased myocardial SOD (P<0.05, P<0.01), Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase activity (P<0.05, P<0.01), but Na(+)-K(+)-ATPase was similar between the two groups (P>0.05). HE staining of the myocardium showed cell swelling and obscure cell boundaries in alcoholism group, especially in chronic alcoholism group. The myocardial structure in puerarin group remained clear and regular. Puerarin can protect from myocardial injuries induced by acute and chronic alcoholism in rats.

Severe Sepsis and Acute Myocardial Dysfunction in an Adolescent with Chlamydia Trachomatis Pelvic Inflammatory Disease: A Case Report.

PubMed

Morgan, Ashley M; Roden, R Claire; Matson, Steven C; Wallace, Grant M; Lange, Hannah L H; Bonny, Andrea E

2018-04-01

Although generally asymptomatic, severe Chlamydia trachomatis (C. trachomatis) infections have been documented. C. trachomatis has been associated with myocarditis as well as sepsis. A 19-year-old girl with type 1 diabetes mellitus developed sudden-onset mental status change and shock after resolution of diabetic ketoacidosis. Abdominal and pelvic imaging showed uterine and adnexal inflammation, and pelvic examination confirmed a diagnosis of pelvic inflammatory disease. The patient was intubated, required vasopressor support, and developed severe biventricular myocardial dysfunction. Infectious myocarditis workup was negative. Nucleic acid amplification testing from vaginal discharge was positive for C. trachomatis and Trichomonas vaginalis and negative for Neisseria gonorrhoeae. C. trachomatis should be considered in the workup of septic shock, particularly in populations at high risk for sexually transmitted infections. Copyright © 2017 North American Society for Pediatric and Adolescent Gynecology. Published by Elsevier Inc. All rights reserved.

Reducing myocardial infarct size: challenges and future opportunities

PubMed Central

Bulluck, Heerajnarain; Yellon, Derek M; Hausenloy, Derek J

2016-01-01

Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is ‘myocardial reperfusion injury’, a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies—however, being able to demonstrate improved clinical outcomes has been elusive. In this article, we review the challenges facing clinical cardioprotection research, and highlight future therapies for reducing MI size and preventing heart failure in patients presenting with STEMI at risk of myocardial reperfusion injury. PMID:26674987

Acute myocardial infarction and stress cardiomyopathy following the Christchurch earthquakes.

PubMed

Chan, Christina; Elliott, John; Troughton, Richard; Frampton, Christopher; Smyth, David; Crozier, Ian; Bridgman, Paul

2013-01-01

Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36 am on 4 September 2010, magnitude 7.1 and at 12:51 pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital was the region's only acute care hospital. It remained functional following both earthquakes. We were able to examine the effects of the 2 earthquakes on acute cardiac presentations. Patients admitted under Cardiology in Christchurch Hospital 3 week prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non cardiac chest pain, arrhythmia and others. There was a significant increase in overall admissions (p<0.003), ST elevation myocardial infarction (p<0.016), and non cardiac chest pain (p<0.022) in the first 2 weeks following the early morning September earthquake. This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6-6.4) in 4 days. There had been 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44-2.62). Statistical analysis showed this to be a significant difference between the earthquakes (p<0.05). The early morning September earthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake caused significantly more stress cardiomyopathy. Two major earthquakes occurring at different times of day differed in their effect on acute cardiac events.

Spontaneous Retro-Orbital Subperiosteal Hemorrhage with Complete Resolution Following Percutaneous Coronary Intervention for Acute Myocardial Infarction.

PubMed

Wu, Hsu-Ping; Tsai, Chia-Jung; Tsai, Jui-Peng; Hung, Chung-Lieh; Kuo, Jen-Yuan; Hou, Charles Jia-Yin

2013-03-01

Among the several treatment strategies available for acute myocardial infarction, primary percutaneous coronary intervention concomitant with antithrombotic agents is the primary treatment used to facilitate coronary reperfusion. However, bleeding can create major complications. Here we have presented a case of acute myocardial infarction treated with reperfusion therapy, after which developed a sudden onset of proptosis, with high intraocular pressure, blurred vision, and ecchymosis of the left eye. Spontaneous retro-orbital subperiosteal hemorrhage, a rare complication, was diagnosed based on those symptoms as noted above, as well as other orbital signs and imaging evaluation. Multiple antithrombotic agents, including antiplatelets, low molecular weight heparin, and glycoprotein IIb/IIIa receptor inhibitor were thought to be the main precipitating factors of this complication. Thereafter, conservative medical treatment was applied. In the following 2 weeks, all the patient's orbital signs resolved gradually without visual impairment. In conclusion, our experience with a rare case of complications arising from reperfusion therapy used to treat myocardial infarction suggests that clinicians should remain vigilant for any hemorrhagic events during acute myocardial infarction treatment. Acute myocardial infarction; Percutaneous coronary intervention; Retro-orbital subperiosteal hemorrhage.

Direct Evidence that Myocardial Insulin Resistance following Myocardial Ischemia Contributes to Post-Ischemic Heart Failure

PubMed Central

Fu, Feng; Zhao, Kun; Li, Jia; Xu, Jie; Zhang, Yuan; Liu, Chengfeng; Yang, Weidong; Gao, Chao; Li, Jun; Zhang, Haifeng; Li, Yan; Cui, Qin; Wang, Haichang; Tao, Ling; Wang, Jing; Quon, Michael J; Gao, Feng

2015-01-01

A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its association with HF are inadequately investigated. This study aims to determine the role of myocardial insulin resistance in ischemic HF and its underlying mechanisms. Male Sprague-Dawley rats subjected to myocardial infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk post-MI. Of note, myocardial insulin sensitivity was decreased as early as 1 wk after MI, which was accompanied by increased production of myocardial TNF-α. Overexpression of TNF-α in heart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI. Treatment of rats with a specific TNF-α inhibitor improved myocardial insulin signaling post-MI. Insulin treatment given immediately following MI suppressed myocardial TNF-α production and improved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling. Moreover, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with controls. In conclusion, MI induces myocardial insulin resistance (without systemic insulin resistance) mediated partly by ischemia-induced myocardial TNF-α overproduction and promotes the development of HF. Our findings underscore the direct and essential role of myocardial insulin signaling in protection against post-ischemic HF. PMID:26659007

Mineralocorticoid receptor antagonists modulate galectin-3 and interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial infarction.

PubMed

Lax, Antonio; Sanchez-Mas, Jesus; Asensio-Lopez, Maria C; Fernandez-Del Palacio, Maria J; Caballero, Luis; Garrido, Iris P; Pastor-Perez, Francisco J; Januzzi, James L; Pascual-Figal, Domingo A

2015-01-01

This study aimed to evaluate the specific role of the 2 available mineralocorticoid receptor antagonists (MRAs), eplerenone and spironolactone, on the modulation of galectin-3 (Gal-3) and interleukin (IL)-33/ST2 signaling in an experimental model of left ventricular systolic dysfunction after acute myocardial infarction (MI). The molecular mechanisms of benefits of MRAs in patients with left ventricular systolic dysfunction after MI not well understood. MI and left ventricular systolic dysfunction were induced by permanent ligation of the anterior coronary artery in 45 male Wistar rats, randomly assigned to no therapy (MI group, n = 15) or to receive MRAs (100 mg/kg/day) for 4 weeks; either eplerenone (n = 15) or spironolactone (n = 15) was used. A sham group was used as a control (n = 8). Elements of the pathway for Gal-3 including transforming growth factor (TGF)-β and SMAD3, as well as that for IL-33/ST2 (including IL-33 and soluble ST2 [sST2]) were analyzed in the infarcted and noninfarcted myocardium by quantitative real-time reverse transcription polymerase chain reaction. Expression of markers of fibrosis (collagen types I and III, tissue inhibitor of metalloproteinase-1) and inflammation (IL-6, tumor necrosis factor-α, monocyte chemotactic protein-1) was also examined. In the infarcted myocardium, compared with sham animals, the MI group had higher concentrations of Gal-3, TGF-β, SMAD3, IL-33, and sST2, as well as higher concentrations of markers of fibrosis and inflammation. Treatment with MRAs down-regulated Gal-3, TGF-β, and SMAD3 and enhanced IL-33/ST2 signaling with lower expression of sST2; protective IL-33 up-regulation was unaffected by MRAs. Modulation of Gal-3 and IL-33/ST2 signaling induced by MRAs correlated with lower expression levels of fibrosis and inflammatory markers. No differences were found between eplerenone and spironolactone. In the noninfarcted myocardium, compared with sham animals, the MI group exhibited a higher expression of

High Serum sTREM-1 Correlates With Myocardial Dysfunction and Predicts Prognosis in Septic Patients.

PubMed

Li, Zhenyu; Zhang, Enyuan; Hu, Yipeng; Liu, Yi; Chen, Bing

2016-06-01

This study aimed to evaluate the predictive and prognostic value of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in patients with myocardial dysfunction induced by severe sepsis and septic shock. A total of 84 patients with severe sepsis and septic shock were enrolled between May 2013 and December 2014.The patients were monitored by pulse indicator continuous cardiac output system and divided into myocardial depression group (cardiac function index [CFI] < 4.1/minute, n = 37) and nonmyocardial depression group (CFI ≥ 4.1/minute, n = 47 ). Additionally, the patients were divided into survival group (n = 40) and nonsurvival group (n = 44) based on 28-day mortality. Hemodynamic parameters and serum sTREM-1, B-type natriuretic peptide (BNP) and cardiac troponin I (cTnI) levels were collected on days 1, 3 and 5 after admission to intensive care unit. (1) The serum values of sTREM-1, BNP and cTnI in myocardial depression group were higher than those in nonmyocardial depression group (P < 0.01); and CFI, cardiac index, stroke volume, global ejection fraction and left ventricular contractility index (dpmax) in myocardial depression group were lower than those in nonmyocardial depression group on day 1 (P < 0.05); (2) serum sTREM-1 negatively correlated with left ventricular ejection fraction, CFI, cardiac index, global ejection fraction and dpmax, and it positively correlated with BNP and cTnI (P < 0.01); (3) the area under the receiver operating characteristics curve for sTREM-1 in the prediction of myocardial depression was 0.671 with a sensitivity of 83.8% and a specificity of 46.8% when cutoff point was 174.5ng/mL, the power of predicting septic depression for sTREM-1 was lower than that of BNP; logistic regression analysis showed that serum sTREM-1 was not an independent predictor of septic myocardial depression; the area under the receiver operating characteristics curve was 0.773 for sTREM-1 in predicting outcome with a sensitivity of 86

Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction

PubMed Central

Lygate, Craig A.; Bohl, Steffen; ten Hove, Michiel; Faller, Kiterie M.E.; Ostrowski, Philip J.; Zervou, Sevasti; Medway, Debra J.; Aksentijevic, Dunja; Sebag-Montefiore, Liam; Wallis, Julie; Clarke, Kieran; Watkins, Hugh; Schneider, Jürgen E.; Neubauer, Stefan

2012-01-01

Aims Increasing energy storage capacity by elevating creatine and phosphocreatine (PCr) levels to increase ATP availability is an attractive concept for protecting against ischaemia and heart failure. However, testing this hypothesis has not been possible since oral creatine supplementation is ineffectual at elevating myocardial creatine levels. We therefore used mice overexpressing creatine transporter in the heart (CrT-OE) to test for the first time whether elevated creatine is beneficial in clinically relevant disease models of heart failure and ischaemia/reperfusion (I/R) injury. Methods and results CrT-OE mice were selected for left ventricular (LV) creatine 20–100% above wild-type values and subjected to acute and chronic coronary artery ligation. Increasing myocardial creatine up to 100% was not detrimental even in ageing CrT-OE. In chronic heart failure, creatine elevation was neither beneficial nor detrimental, with no effect on survival, LV remodelling or dysfunction. However, CrT-OE hearts were protected against I/R injury in vivo in a dose-dependent manner (average 27% less myocardial necrosis) and exhibited greatly improved functional recovery following ex vivo I/R (59% of baseline vs. 29%). Mechanisms contributing to ischaemic protection in CrT-OE hearts include elevated PCr and glycogen levels and improved energy reserve. Furthermore, creatine loading in HL-1 cells did not alter antioxidant defences, but delayed mitochondrial permeability transition pore opening in response to oxidative stress, suggesting an additional mechanism to prevent reperfusion injury. Conclusion Elevation of myocardial creatine by 20–100% reduced myocardial stunning and I/R injury via pleiotropic mechanisms, suggesting CrT activation as a novel, potentially translatable target for cardiac protection from ischaemia. PMID:22915766

Testosterone deficiency prevents left ventricular contractility dysfunction after myocardial infarction.

PubMed

Ribeiro Júnior, R F; Ronconi, K S; Jesus, I C G; Almeida, P W M; Forechi, L; Vassallo, D V; Guatimosim, S; Stefanon, I; Fernandes, A A

2018-01-15

Testosterone may affect myocardial contractility since its deficiency decreases the contraction and relaxation of the heart. Meanwhile, testosterone replacement therapy has raised concerns because it may worsen cardiac dysfunction and remodeling after myocardial infarction (MI). In this study, we evaluate cardiac contractility 60 days after MI in rats with suppressed testosterone. Male Wistar rats underwent bilateral orchidectomy one week before the ligation of the anterior descending left coronary artery. The animals were divided into orchidectomized (OCT); MI; orchidectomized + MI (OCT + MI); orchidectomized + MI + testosterone (OCT + MI + T) and control (Sham) groups. Eight weeks after MI, papillary muscle contractility was analyzed under increasing calcium (0.62, 1.25, 2.5 and 3.75 mM) and isoproterenol (10 -8 to 10 -2  M) concentrations. Ventricular myocytes were isolated for intracellular calcium measurements and assessment of Ca 2+ handling proteins. Contractility was preserved in the orchidectomized animals after myocardial infarction and was reduced when testosterone was replaced (Ca 2+ 3.75 mM: Sham: 608 ± 70 (n = 11); OCT: 590 ± 37 (n = 16); MI: 311 ± 33* (n = 9); OCT + MI: 594 ± 76 (n = 7); OCT + MI + T: 433 ± 38* (n=4), g/g *p < 0.05 vs Sham). Orchidectomy also increased the Ca 2+ transient amplitude of the ventricular myocytes and SERCA-2a protein expression levels. PLB phosphorylation levels at Thr 17 were not different in the orchidectomized animals compared to the Sham animals but were reduced after testosterone replacement. CAMKII phosphorylation and protein nitrosylation increased in the orchidectomized animals. Our results support the view that testosterone deficiency prevents MI contractility dysfunction by altering the key proteins involved in Ca 2+ handling. Copyright © 2017 Elsevier B.V. All rights reserved.

The Olson method for detection of acute myocardial ischemia in patients with coronary occlusion.

PubMed

Lindow, Thomas; Olson, Charles W; Swenne, Cees A; Man, Sumche; Pahlm, Olle

An automated ECG-based method may provide diagnostic support in the management of patients with acute coronary syndrome. The Olson method has previously proved to accurately identify the culprit artery in patients with acute coronary occlusion. The Olson method was applied to 360 patients without acute myocardial ischemia and 52 patients with acute coronary occlusion. This study establishes the normal variation of the Olson wall scores in patients without acute myocardial ischemia, which provides the basis for implementation of the Olson method for triage of patients with acute coronary syndrome. All patients with acute occlusion had Olson wall scores above the upper limit of normal. The Olson method can be used for ischemia detection with very high sensitivity. Future studies are needed to explore specificity in patients with non-ischemic ST elevation. Copyright © 2016 Elsevier Inc. All rights reserved.

Acute myocardial infarction during l-thyroxine therapy in a patient with intermittent changing axis deviation, permanent atrial fibrillation and without significant coronary stenoses.

PubMed

Patanè, Salvatore; Marte, Filippo

2010-01-07

It has been rarely reported intermittent changing axis deviation also occurs during atrial fibrillation. Intermittent changing axis deviation during acute myocardial infarction and changing axis deviation associated with atrial fibrillation and acute myocardial infarction too have been also rarely reported. It has also been reported acute myocardial infarction during l-thyroxine substitution therapy in a patient with elevated levels of free triiodothyronine and without significant coronary artery stenoses. An acute myocardial infarction due to coronary spasm associated with l-thyroxine therapy has also been reported too. We present a case of changing axis deviation during acute myocardial infarction in a 56-year-old Italian woman with permanent atrial fibrillation and l-thyroxine therapy and without significant coronary stenoses. Also this case focuses attention on changing axis deviation in the presence of atrial fibrillation during acute myocardial infarction and on the possible development of acute myocardial infarction without significant coronary stenoses associated with l-thyroxine therapy.

Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents

PubMed Central

Eisenmann, Eric D.; Rorabaugh, Boyd R.; Zoladz, Phillip R.

2016-01-01

Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia–reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions. PMID:27199778

Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents.

PubMed

Eisenmann, Eric D; Rorabaugh, Boyd R; Zoladz, Phillip R

2016-01-01

Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia-reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions.

Increase in electrocardiographic R-waves after revascularization in patients with acute myocardial infarction.

PubMed

Isobe, Satoshi; Takada, Yasuo; Ando, Akitada; Ohshima, Satoru; Yamada, Kiyoyasu; Nanasato, Mamoru; Unno, Kazumasa; Ogawa, Takuo; Kondo, Takahisa; Izawa, Hideo; Inden, Yasuya; Hirai, Makoto; Murohara, Toyoaki

2006-11-01

The physiological mechanism of the increase in the electrocardiographic (ECG) R-wave voltage after revascularization in patients with acute myocardial infarction (MI) needs to be elucidated. One hundred and thirty-eight MI patients (83: anterior MI, 45: inferior MI, 10: lateral MI) underwent ECG and echocardiography in both the acute and subacute phases after emergency revascularization, as well as a resting thallium-201/iodine-123 15-p-iodophenyl-3-(R,S)-methyl pentadecanoic acid myocardial scintigraphy in the acute phase. The total sum of the R-wave voltage (SigmaR) was calculated over multiple leads on ECG for each infarcted lesion. Scintigraphic defect on each tracer was expressed as the percentage (%) defect of the total left ventricular (LV) myocardium. The % defect-discordance on both images in the acute phase and the % increase in SigmaR and the absolute increase in LV ejection fraction from the acute to the subacute phase (DeltaEF) were also calculated. The SigmaR in the subacute phase was significantly greater than that in the acute phase (p<0.0001). The % increase in SigmaR significantly correlated with the DeltaEF (r=0.57, p<0.0001). The % increase in SigmaR also correlated with the % defect-discordance (r=0.68, p<0.0001). The increase in the ECG R-wave voltage reflects not only the improvement in myocardial perfusion but also the presence of salvaged myocardium after revascularization in acute MI patients.

The Role of Echocardiography in Coronary Artery Disease and Acute Myocardial Infarction

PubMed Central

Esmaeilzadeh, Maryam; Parsaee, Mozhgan; Maleki, Majid

2013-01-01

Echocardiography is a non-invasive diagnostic technique which provides information regarding cardiac function and hemodynamics. It is the most frequently used cardiovascular diagnostic test after electrocardiography and chest X-ray. However, in a patient with acute chest pain, Transthoracic Echocardiography is essential both for diagnosing acute coronary syndrome, zeroing on the evaluation of ventricular function and the presence of regional wall motion abnormalities, and for ruling out other etiologies of acute chest pain or dyspnea, including aortic dissection and pericardial effusion. Echocardiography is a versatile imaging modality for the management of patients with chest pain and assessment of left ventricular systolic function, diastolic function, and even myocardial and coronary perfusion and is, therefore, useful in the diagnosis and triage of patients with acute chest pain or dyspnea. This review has focused on the current applications of echocardiography in patients with coronary artery disease and myocardial infarction. PMID:23646042

Myocardial dysfunction occurs prior to changes in ventricular geometry in mice with chronic kidney disease (CKD).

PubMed

Winterberg, Pamela D; Jiang, Rong; Maxwell, Josh T; Wang, Bo; Wagner, Mary B

2016-03-01

Uremic cardiomyopathy is responsible for high morbidity and mortality rates among patients with chronic kidney disease (CKD), but the underlying mechanisms contributing to this complex phenotype are incompletely understood. Myocardial deformation analyses (ventricular strain) of patients with mild CKD have recently been reported to predict adverse clinical outcome. We aimed to determine if early myocardial dysfunction in a mouse model of CKD could be detected using ventricular strain analyses. CKD was induced in 5-week-old male 129X1/SvJ mice through partial nephrectomy (5/6Nx) with age-matched mice undergoing bilateral sham surgeries serving as controls. Serial transthoracic echocardiography was performed over 16 weeks following induction of CKD. Invasive hemodynamic measurements were performed at 8 weeks. Gene expression and histology was performed on hearts at 8 and 16 weeks. CKD mice developed decreased longitudinal strain (-25 ± 4.2% vs. -29 ± 2.3%; P = 0.01) and diastolic dysfunction (E/A ratio 1.2 ± 0.15 vs. 1.9 ± 0.18; P < 0.001) compared to controls as early as 2 weeks following 5/6Nx. In contrast, ventricular hypertrophy was not apparent until 4 weeks. Hearts from CKD mice developed progressive fibrosis at 8 and 16 weeks with gene signatures suggestive of evolving heart failure with elevated expression of natriuretic peptides. Uremic cardiomyopathy in this model is characterized by early myocardial dysfunction which preceded observable changes in ventricular geometry. The model ultimately resulted in myocardial fibrosis and increased expression of natriuretic peptides suggestive of progressive heart failure. © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

The Predictive Role of Serum Triglyceride to High-Density Lipoprotein Cholesterol Ratio According to Renal Function in Patients with Acute Myocardial Infarction

PubMed Central

Woo, Jong Shin; Lee, Tae Won; Ihm, Chun Gyoo; Kim, Yang Gyoon; Moon, Joo Young; Lee, Sang Ho; Jeong, Myung Ho; Jeong, Kyung Hwan

2016-01-01

Objective A high serum triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio has been reported as an independent predictor for cardiovascular events in the general population. However, the prognostic value of this ratio in patients with renal dysfunction is unclear. We examined the association of the TG/HDL-C ratio with major adverse cardiovascular events (MACEs) according to renal function in patients with acute myocardial infarction (AMI). Method This study was based on the Korea Acute Myocardial Infarction Registry database. Of 13,897 patients who were diagnosed with AMI, the study population included the 7,016 patients with available TG/HDL-C ratio data. Patients were stratified into three groups according to their estimated glomerular filtration rate (eGFR), and the TG/HDL-C ratio was categorized into tertiles. We investigated 12-month MACEs, which included cardiac death, myocardial infarction, and repeated percutaneous coronary intervention or coronary artery bypass grafting. Results During the 12-month follow up period, 593 patients experienced MACEs. There was a significant association between the TG/HDL-C ratio and MACEs (p<0.001) in the entire study cohort. Having a TG/HDL-C ratio value in the highest tertile of TG/HDL-C ratio was an independent factor associated with increased risk of MACEs (hazard ratio [HR], 1.56; 95% confidence interval [CI], 1.26–1.93; p<0.001). Then we performed subgroup analyses according to renal function. In patients with normal renal function (eGFR ≥ 90 ml/min/1.73m2) and mild renal dysfunction (eGFR ≥ 60 to < 90ml/min/1.73m2), a higher TG/HDL-C ratio was significantly associated with increased risk of MACEs (HR, 1.64; 95% CI, 1.04–2.60; p = 0.035; and HR, 1.56; 95% CI, 1.14–2.12; p = 0.005, respectively). However, in patients with moderate renal dysfunction (eGFR < 60 ml/min/1.73m2), TG/HDL-C ratio lost its predictive value on the risk of MACEs (HR, 1.23; 95% CI, 0.82–1.83; p = 0.317). Conclusions In

The Predictive Role of Serum Triglyceride to High-Density Lipoprotein Cholesterol Ratio According to Renal Function in Patients with Acute Myocardial Infarction.

PubMed

Kim, Jin Sug; Kim, Weon; Woo, Jong Shin; Lee, Tae Won; Ihm, Chun Gyoo; Kim, Yang Gyoon; Moon, Joo Young; Lee, Sang Ho; Jeong, Myung Ho; Jeong, Kyung Hwan

2016-01-01

A high serum triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio has been reported as an independent predictor for cardiovascular events in the general population. However, the prognostic value of this ratio in patients with renal dysfunction is unclear. We examined the association of the TG/HDL-C ratio with major adverse cardiovascular events (MACEs) according to renal function in patients with acute myocardial infarction (AMI). This study was based on the Korea Acute Myocardial Infarction Registry database. Of 13,897 patients who were diagnosed with AMI, the study population included the 7,016 patients with available TG/HDL-C ratio data. Patients were stratified into three groups according to their estimated glomerular filtration rate (eGFR), and the TG/HDL-C ratio was categorized into tertiles. We investigated 12-month MACEs, which included cardiac death, myocardial infarction, and repeated percutaneous coronary intervention or coronary artery bypass grafting. During the 12-month follow up period, 593 patients experienced MACEs. There was a significant association between the TG/HDL-C ratio and MACEs (p<0.001) in the entire study cohort. Having a TG/HDL-C ratio value in the highest tertile of TG/HDL-C ratio was an independent factor associated with increased risk of MACEs (hazard ratio [HR], 1.56; 95% confidence interval [CI], 1.26-1.93; p<0.001). Then we performed subgroup analyses according to renal function. In patients with normal renal function (eGFR ≥ 90 ml/min/1.73m2) and mild renal dysfunction (eGFR ≥ 60 to < 90ml/min/1.73m2), a higher TG/HDL-C ratio was significantly associated with increased risk of MACEs (HR, 1.64; 95% CI, 1.04-2.60; p = 0.035; and HR, 1.56; 95% CI, 1.14-2.12; p = 0.005, respectively). However, in patients with moderate renal dysfunction (eGFR < 60 ml/min/1.73m2), TG/HDL-C ratio lost its predictive value on the risk of MACEs (HR, 1.23; 95% CI, 0.82-1.83; p = 0.317). In patients with AMI, TG/HDL-C ratio is a

Oestradiol supplement minimises coronary occlusion-induced myocardial infarction and ventricular dysfunction in oophorectomised female rats.

PubMed

Zheng, Xiao-Pu; Ma, Ai-Qun; Dong, An-Ping; Wang, Shun; Jiang, Wen-Hui; Wang, Ting-Zhong; Fan, Fen-Ling; Ling, Shanhong

2011-09-15

Endogenous oestrogen deficiency after menopause is associated with high risk of acute cardiac events and the protection of exogenous oestrogen supplements remains uncertain. This study investigates whether oestrogen therapy protects the heart from ischemic injury in oophorectomised rats. Sexually mature female Sprague-Dawley rats (6 for each group) with bilateral oophorectomy underwent selective ligation (occlusion) of left coronary artery for 4 weeks. 17β-oestradiol (E2) supplements (10 μg, i.m., every other day) were started before (preventive-therapeutic supplement) or after coronary occlusion (therapeutic supplement). In oophorectomised rats plasma levels of E2 declined from 1301 ± 80 to 196 ± 48 pmol/L (p<0.01) and cardiac expression of oestrogen receptors (ER) decreased by ∼60%. E2 supplements recovered the ER expression. Selective ligation of left coronary led myocardial infarction in the left ventricle, with an increase in plasma cardiac troponin I (cTn-I), decrease in systolic blood pressure (SBP), and reduction of left ventricular pressures. Preventive-therapeutic but not therapeutic E2 supplement reduced cTn-I levels (from 21.9 ± 2.0 to 6.0 ± 0.3 ng/mL, p<0.01), minimised infarction (from 37.0 ± 1.2% to 18.1 ± 2.3%, p<0.05), increased SBP (from 82 ± 4.2 to 97 ± 4.4mm Hg, p<0.05), and improved left ventricular end pressures in the oophorectomised rats following coronary occlusion. Postmenopausal (ooporectomised) oestrogen supplement commenced before establishment of myocardial ischemia minimises myocardial infarction and ventricular dysfunction following the coronary artery occlusion. Cellular and molecular mechanisms underlying the cardiac protection of oestrogen therapy remain unclear, in which activation of cardiac ER expression and increasing in circulating CD90(+) stem cells may be involved. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

The prognostic importance of worsening renal function during an acute myocardial infarction on long-term mortality.

PubMed

Amin, Amit P; Spertus, John A; Reid, Kimberly J; Lan, Xiao; Buchanan, Donna M; Decker, Carole; Masoudi, Frederick A

2010-12-01

Although an acute worsening in renal function (WRF) commonly occurs among patients hospitalized for acute myocardial infarction (AMI), its long-term prognostic significance is unknown. We examined predictors of WRF and its association with 4-year mortality. Acute myocardial infarction patients from the multicenter PREMIER study (N=2,098) who survived to hospital discharge were followed for at least 4 years. Worsening in renal function was defined as an increase in creatinine during hospitalization of ≥0.3 mg/dL above the admission value. Correlates of WRF were determined with multivariable logistic regression models and used, along with other important clinical covariates, in Cox proportional hazards models to define the independent association between WRF and mortality. Worsening in renal function was observed in 393 (18.7%) of AMI survivors. Diabetes, left ventricular systolic dysfunction, and a history of chronic kidney disease (documented history of renal failure with baseline creatinine>2.5 mg/dL) were independently associated with WRF. During 4-year follow-up, 386 (18.6%) patients died. Mortality was significantly higher in the WRF group (36.6% vs 14.4% in those without WRF, P<.001). After adjusting for other factors associated with WRF and long-term mortality, including baseline creatinine, WRF was independently associated with a higher risk of death (hazard ratio=1.64, 95% CI 1.23-2.19). Worsening in renal function occurs in approximately 1 of 6 AMI survivors and is independently associated with an adverse long-term prognosis. Further studies on interventions to minimize WRF or to more aggressively treat patients developing WRF should be tested. Copyright © 2010 Mosby, Inc. All rights reserved.

Quality indicators for acute myocardial infarction: A position paper of the Acute Cardiovascular Care Association.

PubMed

Schiele, Francois; Gale, Chris P; Bonnefoy, Eric; Capuano, Frederic; Claeys, Marc J; Danchin, Nicolas; Fox, Keith Aa; Huber, Kurt; Iakobishvili, Zaza; Lettino, Maddalena; Quinn, Tom; Rubini Gimenez, Maria; Bøtker, Hans E; Swahn, Eva; Timmis, Adam; Tubaro, Marco; Vrints, Christiaan; Walker, David; Zahger, Doron; Zeymer, Uwe; Bueno, Hector

2017-02-01

Evaluation of quality of care is an integral part of modern healthcare, and has become an indispensable tool for health authorities, the public, the press and patients. However, measuring quality of care is difficult, because it is a multifactorial and multidimensional concept that cannot be estimated solely on the basis of patients' clinical outcomes. Thus, measuring the process of care through quality indicators (QIs) has become a widely used practice in this context. Other professional societies have published QIs for the evaluation of quality of care in the context of acute myocardial infarction (AMI), but no such indicators exist in Europe. In this context, the European Society of Cardiology (ESC) Acute Cardiovascular Care Association (ACCA) has reflected on the measurement of quality of care in the context of AMI (ST segment elevation myocardial infarction (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI)) and created a set of QIs, with a view to developing programmes to improve quality of care for the management of AMI across Europe. We present here the list of QIs defined by the ACCA, with explanations of the methodology used, scientific justification and reasons for the choice for each measure.

Acute Myocardial Infarction and Stress Cardiomyopathy following the Christchurch Earthquakes

PubMed Central

Chan, Christina; Elliott, John; Troughton, Richard; Frampton, Christopher; Smyth, David; Crozier, Ian; Bridgman, Paul

2013-01-01

Background Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36am on 4 September 2010, magnitude 7.1 and at 12:51pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital was the region's only acute care hospital. It remained functional following both earthquakes. We were able to examine the effects of the 2 earthquakes on acute cardiac presentations. Methods Patients admitted under Cardiology in Christchurch Hospital 3 week prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non cardiac chest pain, arrhythmia and others. Results There was a significant increase in overall admissions (p<0.003), ST elevation myocardial infarction (p<0.016), and non cardiac chest pain (p<0.022) in the first 2 weeks following the early morning September earthquake. This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6–6.4) in 4 days. There had been 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44–2.62). Statistical analysis showed this to be a significant difference between the earthquakes (p<0.05). Conclusion The early morning September earthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake caused significantly more stress cardiomyopathy. Two major earthquakes occurring at different times of day differed in their effect on acute cardiac events. PMID:23844213

Inhibition of CYP2E1 attenuates chronic alcohol intake-induced myocardial contractile dysfunction and apoptosis.

PubMed

Zhang, Rong-Huai; Gao, Jian-Yuan; Guo, Hai-Tao; Scott, Glenda I; Eason, Anna R; Wang, Xiao-Ming; Ren, Jun

2013-01-01

Alcohol intake is associated with myocardial contractile dysfunction and apoptosis although the precise mechanism is unclear. This study was designed to examine the effect of the cytochrome P450 enzyme CYP2E1 inhibition on ethanol-induced cardiac dysfunction. Adult male mice were fed a 4% ethanol liquid or pair-fed control diet for 6weeks. Following 2weeks of diet feeding, a cohort of mice started to receive the CYP2E1 inhibitor diallyl sulfide (100mg/kg/d, i.p.) for the remaining feeding duration. Cardiac function was assessed using echocardiographic and IonOptix systems. Western blot analysis was used to evaluate CYP2E1, heme oxygenase-1 (HO-1), iNOS, the intracellular Ca(2+) regulatory proteins sarco(endo)plasmic reticulum Ca(2+)-ATPase, Na(+)Ca(2+) exchanger and phospholamban, pro-apoptotic protein cleaved caspase-3, Bax, c-Jun-NH(2)-terminal kinase (JNK) and apoptosis signal-regulating kinase (ASK-1). Ethanol led to elevated levels of CYP2E1, iNOS and phospholamban, decreased levels of HO-1 and Na(+)Ca(2+) exchanger, cardiac contractile and intracellular Ca(2+) defects, cardiac fibrosis, overt O(2)(-) production, and apoptosis accompanied with increased phosphorylation of JNK and ASK-1, the effects were significantly attenuated or ablated by diallyl sulfide. Inhibitors of JNK and ASK-1 but not HO-1 inducer or iNOS inhibitor obliterated ethanol-induced cardiomyocyte contractile dysfunction, substantiating a role for JNK and ASK-1 signaling in ethanol-induced myocardial injury. Taken together, these findings suggest that ethanol metabolism through CYP2E1 may contribute to the pathogenesis of alcoholic cardiomyopathy including myocardial contractile dysfunction, oxidative stress and apoptosis, possibly through activation of JNK and ASK-1 signaling. Copyright © 2012 Elsevier B.V. All rights reserved.

Temporal trends in revascularization and outcomes after acute myocardial infarction among the very elderly

PubMed Central

Pagé, Maude; Doucet, Michel; Eisenberg, Mark J.; Behlouli, Hassan; Pilote, Louise

2010-01-01

Background Few data are available on time-related changes in use and outcomes of invasive procedures after acute myocardial infarction in very elderly patients. Our objective was to describe trends in revascularization procedures and outcomes in a provincial cohort of very elderly patients who had experienced acute myocardial infarction. Methods We used a database of hospital discharge summaries to identify all patients aged 80 years or older admitted for acute myocardial infarction in Quebec. We used the provincial database of physicians’ services and medication claims to assess treatment and obtain data on survival. Results Between March 1996 and March 2007, 29 750 patients aged 80 years or older were admitted to hospital for acute myocardial infarction. During this period, use of percutaneous coronary interventions increased from 2.2% to 24.9%, and use of coronary artery bypass graft surgery increased from 0.8% to 3.1%. Evidence-based prescriptions of medication increased over time (p < 0.001). The prevalence of reported comorbidities was higher during the period of 2003–2006 than during the 1996–1999 period. One-year mortality improved over time (46.5% for 1996–1999 v. 40.9% for 2003–2006, p < 0.001) but remained unchanged in the subgroup of patients who did not undergo revascularization. Interpretation The use of revascularization, especially percutaneous coronary interventions, in the very elderly after acute myocardial infarction has been growing at a rapid pace, while the prevalence of reported comorbidities has been increasing in this population. Revascularization procedures are no longer restricted to younger patients. In the context of an aging population, it is imperative to determine whether these changes in practice are cost-effective. PMID:20682731

Diagnostic performance of dark-blood T2-weighted CMR for evaluation of acute myocardial injury.

PubMed

Srichai, Monvadi B; Lim, Ruth P; Lath, Narayan; Babb, James; Axel, Leon; Kim, Daniel

2013-01-01

We compared the image quality and diagnostic performance of 2 fat-suppression methods for black-blood T2-weighted fast spin-echo (FSE), which are as follows: (a) short T1 inversion recovery (STIR; FSE-STIR) and (b) spectral adiabatic inversion recovery (SPAIR; FSE-SPAIR), for detection of acute myocardial injury. Edema-sensitive T2-weighted FSE cardiac magnetic resonance (CMR) imaging is useful in detecting acute myocardial injury but may experience reduced myocardial signal and signal dropout. The SPAIR pulse aims to eliminate artifacts associated with the STIR pulse. A total of 65 consecutive patients referred for CMR evaluation of myocardial structure and function underwent FSE-STIR and FSE-SPAIR, in addition to cine and late gadolinium enhancement (LGE) CMR. T2-weighted FSE images were independently evaluated by 2 readers for image quality and artifacts (Likert scale of 1-5; best-worst) and presence of increased myocardial signal suggestive of edema. In addition, clinical CMR interpretation, incorporating all CMR sequences available, was recorded for comparison. Diagnostic performance of each T2-weighted sequence was measured using recent (<30 days) troponin elevation greater than 2 times the upper limit of normal as the reference standard for acute myocardial injury. Of the 65 patients, there were 21 (32%) with acute myocardial injury. Image quality and artifact scores were significantly better with FSE-SPAIR compared with FSE-STIR (2.15 vs 2.68, P < 0.01; 2.62 vs 3.05, P < 0.01, respectively). The sensitivity, specificity, positive predictive value, and negative predictive value for acute myocardial injury were as follows: 29%, 93%, 67%, and 73% for FSE-SPAIR; 38%, 91%, 67%, and 75% for FSE-STIR; 71%, 98%, 94%, and 88% for clinical interpretation including LGE, T2, and wall motion. There was a statistically significant difference in sensitivity between the clinical interpretation and each of the T2-weighted sequences but not between each T2-weighted sequence

Combined baseline and one-month changes in big endothelin-1 and brain natriuretic peptide plasma concentrations predict clinical outcomes in patients with left ventricular dysfunction after acute myocardial infarction: Insights from the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) study.

PubMed

Olivier, A; Girerd, N; Michel, J B; Ketelslegers, J M; Fay, R; Vincent, J; Bramlage, P; Pitt, B; Zannad, F; Rossignol, P

2017-08-15

Increased levels of neuro-hormonal biomarkers predict poor prognosis in patients with acute myocardial infarction (AMI) complicated by left ventricular systolic dysfunction (LVSD). The predictive value of repeated (one-month interval) brain natriuretic peptides (BNP) and big-endothelin 1 (BigET-1) measurements were investigated in patients with LVSD after AMI. In a sub-study of the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS trial), BNP and BigET-1 were measured at baseline and at 1month in 476 patients. When included in the same Cox regression model, baseline BNP (p=0.0003) and BigET-1 (p=0.026) as well as the relative changes (after 1month) from baseline in BNP (p=0.049) and BigET-1 (p=0.045) were predictive of the composite of cardiovascular death or hospitalization for worsening heart failure. Adding baseline and changes in BigET-1 to baseline and changes in BNP led to a significant increase in prognostic reclassification as assessed by integrated discrimination improvement index (5.0%, p=0.01 for the primary endpoint). Both increased baseline and changes after one month in BigET-1 concentrations were shown to be associated with adverse clinical outcomes, independently from BNP baseline levels and one month changes, in patients after recent AMI complicated with LVSD. This novel result may be of clinical interest since such combined biomarker assessment could improve risk stratification and open new avenues for biomarker-guided targeted therapies. In the present study, we report for the first time in a population of patients with reduced LVEF after AMI and signs or symptoms of congestive HF, that increased baseline values of BNP and BigET-1 as well as a further rise of these markers over the first month after AMI, were independently predictive of future cardiovascular events. This approach may therefore be of clinical interest with the potential of improving risk stratification after AMI with reduced LVEF while

Highly automatic quantification of myocardial oedema in patients with acute myocardial infarction using bright blood T2-weighted CMR

PubMed Central

2013-01-01

Background T2-weighted cardiovascular magnetic resonance (CMR) is clinically-useful for imaging the ischemic area-at-risk and amount of salvageable myocardium in patients with acute myocardial infarction (MI). However, to date, quantification of oedema is user-defined and potentially subjective. Methods We describe a highly automatic framework for quantifying myocardial oedema from bright blood T2-weighted CMR in patients with acute MI. Our approach retains user input (i.e. clinical judgment) to confirm the presence of oedema on an image which is then subjected to an automatic analysis. The new method was tested on 25 consecutive acute MI patients who had a CMR within 48 hours of hospital admission. Left ventricular wall boundaries were delineated automatically by variational level set methods followed by automatic detection of myocardial oedema by fitting a Rayleigh-Gaussian mixture statistical model. These data were compared with results from manual segmentation of the left ventricular wall and oedema, the current standard approach. Results The mean perpendicular distances between automatically detected left ventricular boundaries and corresponding manual delineated boundaries were in the range of 1-2 mm. Dice similarity coefficients for agreement (0=no agreement, 1=perfect agreement) between manual delineation and automatic segmentation of the left ventricular wall boundaries and oedema regions were 0.86 and 0.74, respectively. Conclusion Compared to standard manual approaches, the new highly automatic method for estimating myocardial oedema is accurate and straightforward. It has potential as a generic software tool for physicians to use in clinical practice. PMID:23548176

[Myocardial bridge as the only cause of acute coronary syndrome among the young patients].

PubMed

Miakinkova, Liudmila O; Teslenko, Yurii V; Tsyhanenko, Irina V

2018-01-01

Introduction: Myocardial bridge is an inborn anomaly of coronary artery development, when a part of it is submerged in a myocard, which is pressing the coronary artery to a systola and restrains coronary blood circulation. Generally this feature of coronary blood circulation does not cause any clinical symptoms because the 85% of coronary blood stream of the left ventricle is provided by diastolic filling. Hemodynamic changes in atherosclerosis, tahicardie, hypertrophie of myocard are leading to the manifestation of clinical symptoms of ischemia. The aim: The purpose of the investigation was to discover the features of clinical development of acute coronary syndrome caused by myocardial bridge of young patients without the features of atherosclerotical harm of coronary arteries. Materials and methods: Eight causes of acute coronary syndrome among patients of 28±8,5 years with myocardial bridge which was revealed during coronary angiography, were investigated. Standardized examination and conservative treatment of patients was held, except for three who have got interventional therapy. Results: According to our investigation, myocardial bridge of all investigated patients was located in the middle of the third front interventricular branch of the left coronary artery. Causes of acute coronary syndrome manifestation were tahicardia, spasms of coronary artery, inducted by iatrogenic factors hypertrophie of myocard, hypertrophic cardiomyopatie. Connection between the manifestation of clinical symptoms and length of tunneled segment which did not depend on the level of systolic compres was discovered. The results of conservative and interventional treatment were analyzed. Conclusions: Myocardial bridge can be the cause of myocardial ischemia among patients without signs of coronary atherosclerosis with additional hemodynamic risk facts such as tahicardia, spasms of coronary artery, hypertrophie of myocard. Clinical symptomatology of the acute coronary syndrome is more

Cardiac and Noncardiac Causes of Long-Term Mortality in ST-Segment-Elevation Acute Myocardial Infarction Patients Who Underwent Primary Percutaneous Coronary Intervention.

PubMed

Yamashita, Yugo; Shiomi, Hiroki; Morimoto, Takeshi; Yaku, Hidenori; Furukawa, Yutaka; Nakagawa, Yoshihisa; Ando, Kenji; Kadota, Kazushige; Abe, Mitsuru; Nagao, Kazuya; Shizuta, Satoshi; Ono, Koh; Kimura, Takeshi

2017-01-01

In patients with ST-segment-elevation acute myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention, long-term risks for cardiac and noncardiac death beyond acute phase of STEMI have not been thoroughly evaluated yet. We identified 3942 STEMI patients who had primary percutaneous coronary intervention within 24 hours after onset between January 2005 and December 2007 in the CREDO-Kyoto AMI registry (Coronary Revascularization Demonstrating Outcome study in Kyoto Acute Myocardial Infarction) and evaluated their short-term (within 6-month) and long-term (beyond 6-month) incidences and causes of deaths. The cumulative 5-year incidence of all-cause death in the current study population was 20.4% (cardiac death, 12.2% and noncardiac death, 9.4%, respectively). The vast majority of deaths were cardiac in origin within 6-month (cardiac death, 8.0% and noncardiac death, 0.9%), whereas noncardiac death accounted for nearly two thirds of all-cause death beyond 6-month (cardiac death, 4.6% and noncardiac death, 8.5%). In the stratified analysis according to age, the proportion of noncardiac death was similar regardless of age although the absolute mortality rate was higher with increasing age. By the multivariable Cox regression models, the independent risk factors of all-cause death were advanced age, cardiogenic shock, renal dysfunction, large infarct size, and anterior wall infarction within 6 months after STEMI, and advanced age, previous heart failure, renal dysfunction, and liver cirrhosis beyond 6 months after STEMI, respectively. In STEMI patients who underwent primary percutaneous coronary intervention, the long-term risk for cardiac death was relatively low compared with that for noncardiac death, which accounted for nearly two thirds of all-cause death beyond 6 months. © 2017 American Heart Association, Inc.

Quality of health information on acute myocardial infarction and stroke in the world wide web.

PubMed

Bastos, Ana; Paiva, Dagmara; Azevedo, Ana

2014-01-01

The quality of health information in the Internet may be low. This is a concerning issue in cardiovascular diseases which warrant patient self-management. We aimed to assess the quality of Portuguese websites as a source of health information on acute myocardial infarction and stroke. We used the search terms 'enfarte miocardio' and 'acidente vascular cerebral' (Portuguese terms for myocardial infarction and stroke) on Google(®), on April 5th and 7th 2011, respectively, using Internet Explorer(®). The first 200 URL retrieved in each search were independently visited and Portuguese websites in Portuguese language were selected. We analysed and classified 121 websites for structural characteristics, information coverage and accuracy of the web pages with items defined a priori, trustworthiness in general according to the Health on the Net Foundation and regarding treatments using the DISCERN instrument (48 websites). Websites were most frequently commercial (49.5%), not exclusively dedicated to acute myocardial infarction/ stroke (94.2%), and with information on medical facts (59.5%), using images, video or animation (60.3%). Websites' trustworthiness was low. None of the websites displayed the Health on the Net Foundation seal. Acute myocardial infarction/ stroke websites differed in information coverage but the accuracy of the information was acceptable, although often incomplete. The quality of information on acute myocardial infarction/ stroke in Portuguese websites was acceptable. Trustworthiness was low, impairing users' capability of identifying potentially more reliable content.

[Acute myocardial infarction after wasp sting without anaphylactic reaction].

PubMed

Bongo, Angelo Sante; Fornaro, Gianluigi; Sansa, Mara; Macciò, Sergio; Rognoni, Andrea

2005-03-01

Bites of hymenopterans (bees, wasps and hornets) are very frequent phenomena that can stir up allergical reactions in venom-susceptible patients but that seldom provoke acute myocardial infarction. In the literature we can find case reports of myocardial infarction after bites of hymenopterans, and preceded by an allergic reaction (sometimes with angiographic evidence of undamaged coronary arteries). The pathophysiological determinant seems to be related to the chemical composition of hymenopterans venom, basically made up by vasoactive and thrombogenic substances able to create vasospasm and coronary thrombosis. Our report refers to a 65-year-old male patient without prior cardiological and allergic events who, bitten by a sharm of three bees, complains of an acute large anterior myocardial infarction with angiographic evidence of thrombotic lesion of the proximal left anterior descending artery treated with direct stenting with procedural success, without showing allergical symptoms. The pathophysiological determinant seems to be related to the release of vasoactive amines and thrombogenic substances contained into the hymenopterans venom, the former able to produce vasospasm, the latter able to create diffuse thrombosis. The use of adrenaline itself to counteract the possible systemic allergic reaction appears to advise against the treatment of patients with cardiological symptoms or coronary artery disease and because of its strong vasoactive activity (it leads, in fact, to vasoconstriction) and thrombogenic effects.

Pathophysiology of Myocardial Infarction and Acute Management Strategies.

PubMed

Tibaut, Miha; Mekis, Dusan; Petrovic, Daniel

2017-01-01

On an annual basis, 13.2% of all deaths are attributable to coronary artery disease (CAD), which makes CAD - with 7.4 million deaths - the leading cause of death in the world. In this review, we discuss current knowledge in the pathophysiology of atherosclerosis with its progression to stable CAD and its destabilization and complication with thrombus formation - myocardial infarction (MI). Next, we describe mechanisms of myocardial cell death in MI, the ischemia-reperfusion injury, leftventricular remodeling and complications of MI. Furthermore, we add acute management strategies concentrating on medical therapy, a decision on the reperfusion strategy, timing and cardiac protection by ischemic preconditioning, post-conditioning and remote ischemic conditioning. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Early Treatment With Zofenopril and Ramipril in Combination With Acetyl Salicylic Acid in Patients With Left Ventricular Systolic Dysfunction After Acute Myocardial Infarction: Results of a 5-Year Follow-up of Patients of the SMILE-4 Study.

PubMed

Borghi, Claudio; Omboni, Stefano; Novo, Salvatore; Vinereanu, Dragos; Ambrosio, Giuseppe; Ambrosioni, Ettore

2017-05-01

The SMILE-4 study showed that in patients with left ventricular dysfunction (LVD) after acute myocardial infarction, early treatment with zofenopril plus acetyl salicylic acid is associated with an improved 1-year survival, free from death or hospitalization for cardiovascular (CV) causes, as compared to ramipril plus acetyl salicylic acid. We now report CV outcomes during a 5-year follow-up of the patients of the SMILE-4 study. Three hundred eighty-six of the 518 patients completing the study (51.2%) could be tracked after the study end and 265 could be included in the analysis. During the 5.5 (±2.1) years of follow-up, the primary endpoint occurred in 27.8% of patients originally randomized and treated with zofenopril and in 43.8% of patients treated with ramipril [odds ratio (OR) and 95% confidence interval, 0.65 (0.43-0.98), P = 0.041]. Such a result was achieved through a significantly larger reduction in CV hospitalization under zofenopril [OR: 0.61 (0.37-0.99), P = 0.047], whereas reduction in mortality rate with zofenopril did not achieve statistical significance versus ramipril [OR: 0.75 (0.36-1.59), P = 0.459]. These results were in line with those achieved during the initial 1-year follow-up. Benefits of early treatment of patients with LVD after acute myocardial infarction with zofenopril are sustained over many years as compared to ramipril.

[Acute myocardial infarction in patients with ST-segment elevation myocardial infarction : ESC guidelines 2017].

PubMed

Thiele, H; Desch, S; de Waha, S

2017-12-01

This article gives an update on the management of acute ST-segment elevation myocardial infarction (STEMI) according to the recently released European Society of Cardiology guidelines 2017 and the modifications are compared to the previous STEMI guidelines from 2012. Primary percutaneous coronary intervention (PCI) remains the preferred reperfusion strategy. New guideline recommendations relate to the access site with a clear preference for the radial artery, use of drug-eluting stents over bare metal stents, complete revascularization during the index hospitalization, and avoidance of routine thrombus aspiration. For periprocedural anticoagulation during PCI, bivalirudin has been downgraded. Oxygen treatment should be administered only if oxygen saturation is <90%. In cardiogenic shock, intra-aortic balloon pumps should no longer be used. New recommendations are in place with respect to the duration of dual antiplatelet therapy for patients without bleeding events during the first 12 months. Newly introduced sections cover myocardial infarction with no relevant stenosis of the coronary arteries (MINOCA), the introduction of new indicators for quality of care for myocardial infarction networks and new definitions for the time to reperfusion.

Depression and prognosis following hospital admission because of acute myocardial infarction

PubMed Central

Lauzon, Claude; Beck, Christine A.; Huynh, Thao; Dion, Danielle; Racine, Normand; Carignan, Suzanne; Diodati, Jean G.; Charbonneau, François; Dupuis, Robert; Pilote, Louise

2003-01-01

Background Whether there is an association between depression at the time of acute myocardial infarction and subsequent risk of cardiac complications and death remains controversial. Most studies of this risk factor have been limited to patients of single institutions, and this might account for the varying results. We prospectively evaluated patients admitted to 5 tertiary care and 5 community hospitals and followed them for 1 year to measure the prevalence and prognostic impact of depressive symptoms after acute myocardial infarction. Methods Patients were recruited for the study by trained nurse interviewers who had documented acute myocardial infarction within 2–3 days of admission. The nurses collected information from the medical records and asked study subjects to complete the Beck Depression Inventory questionnaire during their stay in hospital and using a mailed questionnaire 30 days, 6 months and 1 year later. We obtained information on vital status for patients lost to follow-up from a central death registry. Results Of the 587 study subjects, 550 (94%) completed the Beck Depression Inventory at baseline and 191 (35%) had a score of 10 or more, indicating at least mild depression. Rates of depression did not vary over the follow-up period and were similar among patients admitted to tertiary care or community hospitals. Depressed patients were more likely to undergo catheterization (57% v. 47%, 95% confidence interval [CI] around the difference 0.1%–19.6%) and were more likely to undergo percutaneous coronary intervention (32% v. 24%, 95% CI around the difference 0.1%–16.2%) within 30 days of first admission to hospital. Patients with depression on admission had higher rates of a composite of cardiac complications, including recurrent ischemia, infarction or congestive heart failure during their first stay in hospital or readmission for angina, recurrent acute myocardial infarction, congestive heart failure or arrhythmia (adjusted hazard ratio 1

Lipid paradox in acute myocardial infarction-the association with 30-day in-hospital mortality.

PubMed

Cheng, Kai-Hung; Chu, Chih-Sheng; Lin, Tsung-Hsien; Lee, Kun-Tai; Sheu, Sheng-Hsiung; Lai, Wen-Ter

2015-06-01

Elevated low-density lipoprotein cholesterol and triglycerides are major risk factors for coronary artery disease. However, fatty acids from triglycerides are a major energy source, low-density lipoprotein cholesterol is critical for cell membrane synthesis, and both are critical for cell survival. This study was designed to clarify the relationship between lipid profile, morbidity as assessed by Killip classification, and 30-day mortality in patients with acute myocardial infarction. A noninterventional observational study. Coronary care unit in a university hospital. Seven hundred twenty-four patients with acute myocardial infarction in the coronary care program of the Bureau of Health Promotion were analyzed. None. Low-density lipoprotein cholesterol and triglyceride levels were significantly lower in high-Killip (III+IV) patients compared with low-Killip (I+II) patients and in those who died compared with those who survived beyond 30 days (both p<0.001). After adjustment for risk factors, low-density lipoprotein cholesterol less than 62.5 mg/dL and triglycerides less than 110 mg/dL were identified as optimal threshold values for predicting 30-day mortality and were associated with hazard ratios of 1.65 (95% CI, 1.18-2.30) and 5.05 (95% CI, 1.75-14.54), and the actual mortality rates were 23% in low low-density lipoprotein, 6% in high low-density lipoprotein, 14% in low triglycerides, and 3% in high triglycerides groups, respectively. To test the synergistic effect, high-Killip patients with triglycerides less than 62.5 mg/dL and low-density lipoprotein cholesterol less than 110 mg/dL had a 10.9-fold higher adjusted risk of mortality than low-Killip patients with triglycerides greater than or equal to 62.5 mg/dL and low-density lipoprotein cholesterol greater than or equal to 110 mg/dL (p<0.001). The lipid paradox also improved acute myocardial infarction short-term outcomes prediction on original Killip and thrombolytic in myocardial infarction scores. Low low

Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute myocardial infarction: results from the METOCARD-CNIC trial (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction).

PubMed

Pizarro, Gonzalo; Fernández-Friera, Leticia; Fuster, Valentin; Fernández-Jiménez, Rodrigo; García-Ruiz, José M; García-Álvarez, Ana; Mateos, Alonso; Barreiro, María V; Escalera, Noemí; Rodriguez, Maite D; de Miguel, Antonio; García-Lunar, Inés; Parra-Fuertes, Juan J; Sánchez-González, Javier; Pardillos, Luis; Nieto, Beatriz; Jiménez, Adriana; Abejón, Raquel; Bastante, Teresa; Martínez de Vega, Vicente; Cabrera, José A; López-Melgar, Beatriz; Guzman, Gabriela; García-Prieto, Jaime; Mirelis, Jesús G; Zamorano, José Luis; Albarrán, Agustín; Goicolea, Javier; Escaned, Javier; Pocock, Stuart; Iñiguez, Andrés; Fernández-Ortiz, Antonio; Sánchez-Brunete, Vicente; Macaya, Carlos; Ibanez, Borja

2014-06-10

The goal of this trial was to study the long-term effects of intravenous (IV) metoprolol administration before reperfusion on left ventricular (LV) function and clinical events. Early IV metoprolol during ST-segment elevation myocardial infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percutaneous coronary intervention (pPCI). The METOCARD-CNIC (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction) trial recruited 270 patients with Killip class ≤II anterior STEMI presenting early after symptom onset (<6 h) and randomized them to pre-reperfusion IV metoprolol or control group. Long-term magnetic resonance imaging (MRI) was performed on 202 patients (101 per group) 6 months after STEMI. Patients had a minimal 12-month clinical follow-up. Left ventricular ejection fraction (LVEF) at the 6 months MRI was higher after IV metoprolol (48.7 ± 9.9% vs. 45.0 ± 11.7% in control subjects; adjusted treatment effect 3.49%; 95% confidence interval [CI]: 0.44% to 6.55%; p = 0.025). The occurrence of severely depressed LVEF (≤35%) at 6 months was significantly lower in patients treated with IV metoprolol (11% vs. 27%, p = 0.006). The proportion of patients fulfilling Class I indications for an implantable cardioverter-defibrillator (ICD) was significantly lower in the IV metoprolol group (7% vs. 20%, p = 0.012). At a median follow-up of 2 years, occurrence of the pre-specified composite of death, heart failure admission, reinfarction, and malignant arrhythmias was 10.8% in the IV metoprolol group versus 18.3% in the control group, adjusted hazard ratio (HR): 0.55; 95% CI: 0.26 to 1.04; p = 0.065. Heart failure admission was significantly lower in the IV metoprolol group (HR: 0.32; 95% CI: 0.015 to 0.95; p = 0.046). In patients with anterior Killip class ≤II STEMI undergoing pPCI, early IV metoprolol before reperfusion resulted in higher long-term LVEF, reduced incidence of severe LV systolic dysfunction

Use of orbital atherectomy in acute myocardial infarction via the transradial approach

PubMed Central

Mowakeaa, Samer; Snyder, Branden; Kakouros, Nikolaos

2016-01-01

Severe coronary artery calcifications pose an ongoing challenge when performing percutaneous coronary interventions, resulting in an increased likelihood of procedural complications. Orbital atherectomy (OA) has emerged as a promising technology that helps improve outcomes in this complex patient population. Its safety and efficacy are yet to be demonstrated in the setting of acute myocardial infarction. We present a case of a patient with acute ST-elevation myocardial infarction (STEMI) evaluated with emergent transradial coronary angiography. The culprit lesion was a severely stenotic, heavily calcified, segment of the right coronary artery. The use of OA facilitated lesion expansion and implantation of a drug-eluting stent. Although OA should be considered as contraindicated for the management of soft-ruptured plaque, which accounts for the majority of STEMI presentations, it may be well applied to the small subset of patients with calcified nodule pathology, even in the acute setting. PMID:28180008

Revelation of changing axis deviation at the end of atrial fibrillation during acute myocardial infarction.

PubMed

Patanè, Salvatore; Marte, Filippo

2011-05-19

It has been rarely reported changing axis deviation also during atrial fibrillation or atrial flutter. Changing axis deviation has been also rarely reported during acute myocardial infarction associated with atrial fibrillation too. We present a case of a 49-year-old Italian man with revelation of changing axis deviation at the end of atrial fibrillation during acute myocardial infarction. Also this case focuses attention on changing axis deviation. Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.

Chest pain emergency centers: improving acute myocardial infarction care.

PubMed

Ornato, J P

1999-08-01

Uncertainty and delay are common in the diagnosis of acute coronary syndromes (ACS). In the last 20 years, the need for faster, more accurate, and more cost-effective diagnosis gave rise to the concept of specialized treatment of patients with chest pain in emergency departments (EDs). The original strategy dedicated a separate section of the ED and a nursing staff to the task of rapid intervention in patients with acute myocardial infarction (MI) and triage of low-risk patients. Chest pain centers grew quickly in popularity but evolved with a variety of goals, staffing plans, diagnostic resources, and levels of commitment. There existing centers--the University of Cincinnati Heart ER, Brigham and Women's Hospital, and the Medical College of Virginia--have implemented chest pain strategies with the common aims of (1) screening for the entire spectrum of coronary artery disease, (2) avoiding unnecessary admissions, and (3) using multiple diagnostic modalities. Yet, they differ in the specifics of their approaches and diagnostic methods (e.g., echocardiography vs. treadmill vs. myocardial perfusion imaging). The safety and cost effectiveness of these centers are discussed.

[Diagnostics of acute myocardial infarction in elderly patients].

PubMed

Bahrmann, P; Heppner, H J; Bahrmann, A; Christ, M; Bertsch, T; Sieber, C C

2011-06-01

The early diagnosis of an acute myocardial infarction (MI) is improved by the introduction of novel high-sensitivity troponin assays. These assays can measure low level myocardial injury not detectable by standard troponin assays. Especially in older patients who appear to have a higher basal troponin level, the results must always be judged in the context of the medical history, physical examination, electrocardiogram (ECG) and any further findings. Even small increases in high-sensitivity troponin indicate increased risk for death or MI during follow-up. In the case of MI an invasive strategy results in better survival rates compared with conservative therapy but at the expense of an increased risk of bleeding in elderly patients. This article provides an overview on the diagnosis of MI in elderly patients.

Diagnostic usefulness of the oedema-infarct ratio to differentiate acute from chronic myocardial damage using magnetic resonance imaging.

PubMed

Yamada, Kiyoyasu; Isobe, Satoshi; Suzuki, Susumu; Kinoshita, Kousuke; Yokouchi, Kazuhiko; Iwata, Hirokazu; Ohshima, Satoru; Hirai, Makoto; Sawada, Ken; Murohara, Toyoaki

2012-04-01

To differentiate acute from chronic damage to the myocardium in patients with myocardial infarction (MI) using DE and T2w MR. Short-axis T2w and DE MR images were acquired twice after the onset of MI in 36 patients who successfully underwent emergency coronary revascularisation. The areas of infarct and oedema were measured. The oedema-infarct ratio (O/I) of the left ventricular area was calculated by dividing the oedema by the infarct area. The oedema size on T2w MR was significantly larger than the infarct size on DE MR in the acute phase. Both the oedema size on T2w MR and the infarct size on DE MR in the acute phase were significantly larger than those in the chronic phase. The O/I was significantly greater in the acute phase compared with that in the chronic phase (P < 0.05). An analysis of relative cumulative frequency distributions revealed an O/I of 1.4 as a cut-off value for differentiating acute from chronic myocardial damage with the sensitivity, specificity, and accuracy of 85.1%, 82.7% and 83.9%, respectively. The oedema-infarct ratio may be a useful index in differentiating acute from chronic myocardial damage in patients with MI. MR can differentiate reversible from irreversible myocardial damage after myocardial infarction. MR is a useful modality to noninvasively differentiate the infarct stages. The O/I is an important index to decide therapeutic strategies.

Diastolic dysfunction in the critically ill patient.

PubMed

Suárez, J C; López, P; Mancebo, J; Zapata, L

2016-11-01

Left ventricular diastolic dysfunction is a common finding in critically ill patients. It is characterized by a progressive deterioration of the relaxation and the compliance of the left ventricle. Two-dimensional and Doppler echocardiography is a cornerstone in its diagnosis. Acute pulmonary edema associated with hypertensive crisis is the most frequent presentation of diastolic dysfunction critically ill patients. Myocardial ischemia, sepsis and weaning failure from mechanical ventilation also may be associated with diastolic dysfunction. The treatment is based on the reduction of pulmonary congestion and left ventricular filling pressures. Some studies have found a prognostic role of diastolic dysfunction in some diseases such as sepsis. The present review aims to analyze thoroughly the echocardiographic diagnosis and the most frequent scenarios in critically ill patients in whom diastolic dysfunction plays a key role. Copyright © 2016 Elsevier España, S.L.U. y SEMICYUC. All rights reserved.

Atrial fibrillation and acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism and erythrocytosis.

PubMed

Patanè, Salvatore; Marte, Filippo

2010-11-05

Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. It has been reported that sub-clinical hyperthyroidism is not associated with CHD or mortality from cardiovascular causes but is sufficient to induce arrhythmias including atrial fibrillation and atrial flutter. Moreover increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. It has been also reported an acute myocardial infarction with normal coronary arteries associated with iatrogenic hyperthyroidism and with a myocardial bridge too. It has been also reported an acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism. Furthermore it has been reported that at highly increased hematocrit levels patients may experience hyperviscosity symptoms. We present a case of atrial fibrillation and acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism and erythrocytosis. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism. Copyright © 2008 Elsevier Ireland Ltd. All rights reserved.

Painless acute myocardial infarction on Mount Kilimanjaro

PubMed Central

Jamal, Nasiruddin; Rajhy, Mubina; Bapumia, Mustaafa

2016-01-01

An individual experiencing dyspnoea or syncope at high altitude is commonly diagnosed to have high-altitude pulmonary edema or cerebral edema. Acute myocardial infarction (AMI) is generally not considered in the differential diagnosis. There have been very rare cases of AMI reported only from Mount Everest. We report a case of painless ST segment elevation myocardial infarction (STEMI) that occurred while climbing Mount Kilimanjaro. A 51-year-old man suffered dyspnoea and loss of consciousness near the mountain peak, at about 5600 m. At a nearby hospital, he was treated as a case of high-altitude pulmonary edema. ECG was not obtained. Two days after the incident, he presented to our institution with continued symptoms of dyspnoea, light-headedness and weakness, but no pain. He was found to have inferior wall and right ventricular STEMI complicated by complete heart block. He was successfully managed with coronary angioplasty, with good recovery. PMID:26989121

Lingual Haematoma due to Tenecteplase in a Patient with Acute Myocardial Infarction

PubMed Central

Bal, Muhlis; Salturk, Ziya; Ateş, Ahmet Hakan; Yağcı, Serkan; Coşkun Bal, Gökçen

2013-01-01

The use of intravenous thrombolytic agents has revolutionised the treatment of acute myocardial infarction. However, the improvement in mortality rate achieved with these drugs is tempered by the risk of serious bleeding complications, including intracranial haemorrhage. Tenecteplase is a genetically engineered mutant tissue plasminogen activator. Haemorrhagic complications of tissue plasminogen activator (tPA) are well known. Compared to other tPAs, tenecteplase use leads to lower rates of bleeding complications. Here, we report a case of unusual site of spontaneous bleeding, intralingual haematoma during tenecteplase therapy following acute myocardial infarction, which caused significant upper airway obstruction and required tracheotomy to maintain the patient's airway. Clinical dilemmas related to securing the airway or reversing the effects of tissue plasminogen activator are discussed. PMID:23862086

Detrimental effects of acute hyperglycaemia on the rat heart.

PubMed

Mapanga, R F; Joseph, D; Symington, B; Garson, K-L; Kimar, C; Kelly-Laubscher, R; Essop, M Faadiel

2014-03-01

Hyperglycaemia is an important risk factor for acute myocardial infarction. It can lead to increased induction of non-oxidative glucose pathways (NOGPs) - polyol and hexosamine biosynthetic pathways, advanced glycation end products and protein kinase C - that may contribute to cardiovascular diseases onset. However, the precise underlying mechanisms remain poorly understood. Here we hypothesized that acute hyperglycaemia increases myocardial oxidative stress and NOGP activation resulting in cardiac dysfunction during ischaemia-reperfusion and that inhibition of, and/or shunting flux away from NOGPs [by benfotiamine (BFT) treatment], leads to cardioprotection. We employed several experimental systems: (i) Isolated rat hearts were perfused ex vivo with Krebs-Henseleit buffer containing 33 mm glucose vs. controls (11 mm glucose) ± global ischaemia and reperfusion ± BFT (first 20 min of reperfusion); (ii) Infarct size determination as per the ischaemic protocol, but with regional ischaemia and reperfusion ± BFT treatment; in separate experiments, NOGP inhibitors were also employed for (i) and (ii); and (iii) In vivo coronary ligations performed on streptozotocin-treated rats ± BFT treatment (early reperfusion). Acute hyperglycaemia generated myocardial oxidative stress, NOGP activation and apoptosis, but caused no impairment of cardiac function during pre-ischaemia, thereby priming hearts for later damage. Following ischaemia-reperfusion (under hyperglycaemic conditions), such effects were exacerbated together with cardiac contractile dysfunction. Moreover, inhibition of respective NOGPs and shunting away by BFT treatment (in part) improved cardiac function during ischaemia-reperfusion. Coordinate NOGP activation in response to acute hyperglycaemia results in contractile dysfunction during ischaemia-reperfusion, allowing for the development of novel cardioprotective agents. © 2013 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

Approach to chest pain and acute myocardial infarction.

PubMed

Pandie, S; Hellenberg, D; Hellig, F; Ntsekhe, M

2016-03-01

Patient history, physical examination, 12-lead electrocardiogram (ECG) and cardiac biomarkers are key components of an effective chest pain assessment. The first priority is excluding serious chest pain syndromes, namely acute coronary syndromes (ACSs), aortic dissection, pulmonary embolism, cardiac tamponade and tension pneumothorax. On history, the mnemonic SOCRATES (Site Onset Character Radiation Association Time Exacerbating/relieving factor and Severity) helps differentiate cardiac from non-cardiac pain. On examination, evaluation of vital signs, evidence of murmurs, rubs, heart failure, tension pneumothoraces and chest infections are important. A 12-lead ECG should be interpreted within 10 minutes of first medical contact, specifically to identify ST elevation myocardial infarction (STEMI). High-sensitivity troponins improve the rapid rule-out of myocardial infarction (MI) and confirmation of non-ST elevation MI (NSTEMI). ACS (STEMI and NSTEMI/unstable anginapectoris (UAP)) result from acute destabilisation of coronary atheroma with resultant complete (STEMI) or subtotal (NSTEMI/UAP) thrombotic coronary occlusion. The management of STEMI patients includes providing urgent reperfusion: primary percutaneous coronary intervention(PPCI) if available, deliverable within 60 - 120 minutes, and fibrinolysis if PPCI is not available. Essential adjunctive therapies include antiplatelet therapy (aspirin, P2Y12 inhibitors), anticoagulation (heparin or low-molecular-weight heparin) and cardiac monitoring.

Risk factors of acute myocardial infarction in middle-aged and adolescent people (< 45 years) in Yantai.

PubMed

Du, Hong; Dong, Chang-Yan; Lin, Qiao-Yan

2015-09-29

Yantai is a developed medium-sized coastal city in Eastern China, having a population of 1.6845 million. With the development of economy, some middle-aged and adolescent people (< 45 years) devote themselves to work and suffer from greater stress, which makes them ignore their own health. Moreover, they have unhealthy lifestyles and lack the knowledge of cardiovascular risk factors. To identify the risk factors for first acute myocardial infarction in middle-aged and adolescent people in Yantai, a developed medium-sized coastal city in Eastern China. A total of 154 consecutive patients with first acute myocardial infarction (< 45 years), were enrolled in case group, and 462 patients without myocardial infarction were enrolled in control group. Three controls with the same sex and age were matched to each case. The risk factors were identified with univariate and multivariate analysis. Unhealthy food habit (eating seafood and meanwhile drinking beer), hypertension, current smokers, self-perceived stress, diabetes mellitus, obesity, sleep insufficience, hypercholesterolaemia and fatigue were independent risk factors for first acute myocardial infarction (P < 0.05). Besides those recognized risk factors for cardiovascular disease (hypertension, hypercholesterolemia, diabetes mellitus and smoking), eating seafood and meanwhile drinking beer, self-perceived stress, sleep insufficience, obesity and fatigue were also the risk factors for first acute myocardial infarction in middle-aged and adolescent people in Yantai.

Two-dimensional color tissue Doppler imaging detects myocardial dysfunction before occurrence of hypertrophy in a young Maine Coon cat.

PubMed

Chetboul, Valerie; Sampedrano, Carolina Carlos; Gouni, Vassiliki; Nicolle, Audrey P; Pouchelon, Jean-Louis

2006-01-01

A 20-month-old healthy male Maine Coon cat was referred for a cardiovascular evaluation. Physical examination and electrocardiogram were normal. The end-diastolic subaortic interventricular septal thickness (6 mm; reference range: < or = 6mm) and the mitral flow late diastolic velocity (0.89 m/s; reference range: 0.2-0.8m/s) were within the upper ranges. However, M-mode echocardiography did not reveal any sign of hypertrophic cardiomyopathy (HCM). Tissue Doppler imaging (TDI) identified a marked left ventricular free wall dysfunction characterized by decreased myocardial velocities in early diastole, increased myocardial velocities in late diastole and the presence of postsystolic contractions both at the base and the apex for the longitudinal motion. One year later, the diagnosis of HCM was confirmed by conventional echocardiography and the cat died suddenly 2 months later. This report demonstrates for the first time in spontaneous HCM the sensitivity of TDI for early diagnosis of myocardial dysfunction and suggests that TDI should form part of the screening techniques for early diagnosis of feline HCM.

Effects of Chronic and Acute Zinc Supplementation on Myocardial Ischemia-Reperfusion Injury in Rats.

PubMed

Ozyıldırım, Serhan; Baltaci, Abdulkerim Kasim; Sahna, Engin; Mogulkoc, Rasim

2017-07-01

The present study aims to explore the effects of chronic and acute zinc sulfate supplementation on myocardial ischemia-reperfusion injury in rats. The study registered 50 adult male rats which were divided into five groups in equal numbers as follows: group 1, normal control; group 2, sham; group 3, myocardial ischemia reperfusion (My/IR): the group which was fed on a normal diet and in which myocardial I/R was induced; group 4, myocardial ischemia reperfusion + chronic zinc: (5 mg/kg i.p. zinc sulfate for 15 days); and group 5, myocardial ischemia reperfusion + acute zinc: the group which was administered 15 mg/kg i.p. zinc sulfate an hour before the operation and in which myocardial I/R was induced. The collected blood and cardiac tissue samples were analyzed using spectrophotometric method to determine levels of MDA, as an indicator of tissue injury, and GSH, as an indicator of antioxidant activity. The highest plasma and heart tissue MDA levels were measured in group 3 (p < 0.05). Group 5 had lower MDA values than group 3, while group 4 had significantly lower MDA values than groups 3 and 5 (p < 0.05). The highest erythrocyte GSH values were found in group 4 (p < 0.05). Erythrocyte GSH values in group 5 were higher than those in group 3 (p < 0.05). The highest GSH values in heart tissue were measured in group 4 (p < 0.05). The results of the study reveal that the antioxidant activity inhibited by elevated oxidative stress in heart ischemia reperfusion in rats is restored partially by acute zinc administration and markedly by chronic zinc supplementation.

Depressive disorder and gastrointestinal dysfunction after myocardial infarct are associated with abnormal tryptophan-5-hydroxytryptamine metabolism in rats

PubMed Central

Liu, Chunyan; Wang, Yangang

2017-01-01

In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the somatic, cognitive

Depressive disorder and gastrointestinal dysfunction after myocardial infarct are associated with abnormal tryptophan-5-hydroxytryptamine metabolism in rats.

PubMed

Lu, Xiaofang; Wang, Yuefen; Liu, Chunyan; Wang, Yangang

2017-01-01

In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the somatic, cognitive

T-Wave Abnormality as Electrocardiographic Signature of Myocardial Edema in Non-ST-Elevation Acute Coronary Syndromes.

PubMed

Cardona, Andrea; Zareba, Karolina M; Nagaraja, Haikady N; Schaal, Stephen F; Simonetti, Orlando P; Ambrosio, Giuseppe; Raman, Subha V

2018-01-26

T-wave abnormalities are common during the acute phase of non-ST-segment elevation acute coronary syndromes, but mechanisms underlying their occurrence are unclear. We hypothesized that T-wave abnormalities in the presentation of non-ST-segment elevation acute coronary syndromes correspond to the presence of myocardial edema. Secondary analysis of a previously enrolled prospective cohort of patients presenting with non-ST-segment elevation acute coronary syndromes was conducted. Twelve-lead electrocardiography (ECG) and cardiac magnetic resonance with T2-weighted imaging were acquired before invasive coronary angiography. ECGs were classified dichotomously (ie, ischemic versus normal/nonischemic) and nominally according to patterns of presentation: no ST- or T-wave abnormalities, isolated T-wave abnormality, isolated ST depression, ST depression+T-wave abnormality. Myocardial edema was determined by expert review of T2-weighted images. Of 86 subjects (65% male, 59.4 years), 36 showed normal/nonischemic ECG, 25 isolated T-wave abnormalities, 11 isolated ST depression, and 14 ST depression+T-wave abnormality. Of 30 edema-negative subjects, 24 (80%) had normal/nonischemic ECGs. Isolated T-wave abnormality was significantly more prevalent in edema-positive versus edema-negative subjects (41.1% versus 6.7%, P =0.001). By multivariate analysis, an ischemic ECG showed a strong association with myocardial edema (odds ratio 12.23, 95% confidence interval 3.65-40.94, P <0.0001). Among individual ECG profiles, isolated T-wave abnormality was the single strongest predictor of myocardial edema (odds ratio 23.84, 95% confidence interval 4.30-132, P <0.0001). Isolated T-wave abnormality was highly specific (93%) but insensitive (43%) for detecting myocardial edema. T-wave abnormalities in the setting of non-ST-segment elevation acute coronary syndromes are related to the presence of myocardial edema. High specificity of this ECG alteration identifies a change in ischemic

Personality factors and depression as predictors of hospital-based health care utilization following acute myocardial infarction.

PubMed

Schlyter, Mona; Östman, Margareta; Engström, Gunnar; André-Petersson, Lena; Tydén, Patrik; Leosdottir, Margrét

2017-04-01

Whether personality factors and depressive traits affect patients' utilization of health care following an acute myocardial infarction is relatively unknown. The aim of this study was to examine whether hospital-based health care utilization after a myocardial infarction was correlated with patients' personality factors and depressive symptoms. We studied 366 myocardial infarction patients admitted to Malmö University Hospital between 2002 and 2005 who subsequently participated in a cardiac rehabilitation programme. The patients were followed for two years after their index event. We investigated whether personality factors and depressive traits were correlated with the participants' health care utilization, defined as a) out-patient Cardiology visits and phone calls to a physician, nurse or a social worker, and b) acute visits or admissions to the Emergency or Cardiology Departments, using negative binominal regression analysis. In unadjusted comparisons neuroticism predicted more out-patient contacts. This significance remained after adjusting for age, sex, smoking, alcohol consumption and size of the myocardial infarction (measured as max level on troponin-I and left ventricular ejection fraction). There were no significant correlations between other personality factors or depression and out-patient contacts. None of the personality factors or depression predicted acute admissions. Apart from neuroticism, personality factors did not explain utilization of health care in terms of Cardiology out-patient contacts or acute admissions in myocardial infarction patients participating in a cardiac rehabilitation programme. Neither did depressive symptoms predict more health care utilization. This might indicate a robust cardiac rehabilitation programme offered to the study subjects, minimizing the need for additional health care contacts.

Cannabis: a trigger for acute myocardial infarction? A case report.

PubMed

Cappelli, Francesco; Lazzeri, Chiara; Gensini, Gian Franco; Valente, Serafina

2008-07-01

Cannabis smoking is consistently increasing in Europe and after alcohol it is the most common recreational drug in the western world. Users and lay people believe that marijuana or hashish is safe. Over the past four decades, however, it has been well established that cannabis has pathophysiological effects on the cardiovascular system. Information concerning the link between cannabis consumption and myocardial infarction is limited and existing data are controversial on this topic. In our case report, we describe a case of a young man who after smoking marijuana experienced ST elevation myocardial infarction caused by acute thrombosis of the descending artery, submitted to efficacious primary coronary angioplasty.

Establishment of a canine model of acute pulmonary embolism with definite right ventricular dysfunction through introduced autologous blood clots.

PubMed

Zhao, Lin-Bo; Jia, Zhen-Yu; Lu, Guang-Dong; Zhu, Yin-Su; Jing, Lei; Shi, Hai-Bin

2015-04-01

To establish a canine model of acute pulmonary embolism (PE) with right ventricular (RV) dysfunction using autologous blood clots and evaluate by echocardiography and contrast-enhanced Computed Tomography (CT). Autologous blood clots formed in vitro were introduced sequentially into the pulmonary arteries of eight healthy mixed-breed dogs while monitoring pulmonary and systemic hemodynamic function. Blood clots were injected until the mean pulmonary artery pressure (MPAP) reached two-three times the baseline pressure, which was maintained up to 1 hour. The RV function was assessed by echocardiography and ECG-gated dual-source contrast CT. All animals survived the imaging procedure. The post-injection pulmonary angiograms showed extensive PE, and MPAP increased from 16.50±2.45 mmHg to 43.13±4.91 mmHg (P<0.001). On echocardiography, the RV fractional area change decreased from 42.06±3.36 to 27.96±3.54 (P<0.001), and the RV myocardial performance increased from 0.20±0.05 to 0.63±0.16 (P<0.001). On CT, the RV end-systolic volume increased from 11.11±1.81 ml to 24.71±4.60 ml (P<0.001), RV end-diastolic volume from 20.73±2.83 ml to 34.63±5.76 ml (P<0.001), and the four-chamber RV/left ventricular diameter ratio from 0.38±0.07 to 0.81±0.14 (P<0.001). Acute PE with RV dysfunction was established in a large animal model through controlled injection of autologous blood clots, which may be useful for developing and evaluating new therapeutic approaches for acute PE with RV dysfunction. Copyright © 2015 Elsevier Ltd. All rights reserved.

Evaluation of heart perfusion in patients with acute myocardial infarction using dynamic contrast-enhanced magnetic resonance imaging.

PubMed

Nielsen, Gitte; Fritz-Hansen, Thomas; Dirks, Christina G; Jensen, Gorm B; Larsson, Henrik B W

2004-09-01

To investigate the diagnostic ability of quantitative magnetic resonance imaging (MRI) heart perfusion in acute heart patients, a fast, multislice dynamic contrast-enhanced MRI sequence was applied to patients with acute myocardial infarction. Seven patients with acute transmural myocardial infarction were studied using a Turbo-fast low angle shot (FLASH) MRI sequence to monitor the first pass of an extravascular contrast agent (CA), gadolinium diethylene triamine pentaacetic acid (Gd-DTPA). Quantitation of perfusion, expressed as Ki (mL/100 g/minute), in five slices, each having 60 sectors, provided an estimation of the severity and extent of the perfusion deficiency. Reperfusion was assessed both by noninvasive criteria and by coronary angiography (CAG). The Ki maps clearly delineated the infarction in all patients. Thrombolytic treatment was clearly beneficial in one case, but had no effect in the two other cases. Over the time-course of the study, normal perfusion values were not reestablished following thrombolytic treatment in all cases investigated. This study shows that quantitative MRI perfusion values can be obtained from acutely ill patients following acute myocardial infarction. The technique provides information on both the volume and severity of affected myocardial tissue, enabling the power of treatment regimes to be assessed objectively, and this approach should aid individual patient stratification and prognosis. Copyright 2004 Wiley-Liss, Inc.

Endoplasmic reticulum Chaperon Tauroursodeoxycholic Acid Alleviates Obesity-Induced Myocardial Contractile Dysfunction

PubMed Central

Ceylan-Isik, Asli F.; Sreejayan, Nair; Ren, Jun

2010-01-01

ER stress is involved in the pathophysiology of obesity although little is known about the role of ER stress on obesity-associated cardiac dysfunction. This study was designed to examine the effect of ER chaperone tauroursodeoxycholic acid (TUDCA) on obesity-induced myocardial dysfunction. Adult lean and ob/ob obese mice were treated TUDCA (50 mg/kg/d, p.o.) or vehicle for 5 wks. Oral glucose tolerance test (OGTT) was performed. Echocardiography, cardiomyocyte contractile and intracellular Ca2+ properties were assessed. Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity and protein expression of intracellular Ca2+ regulatory proteins were measured using 45Ca2+ uptake and Western blot analysis, respectively. Insulin signaling, ER stress markers and HSP90 were evaluated. Our results revealed that chronic TUDCA treatment lower systolic blood pressure and lessened glucose intolerance in obese mice. Obesity led to increased diastolic diameter, cardiac hypertrophy, compromised fractional shortening, cardiomyocyte contractile (peak shortening, maximal velocity of shortening/relengthening, and duration of contraction/relaxation) and intracellular Ca2+ properties, all of which were significantly attenuated by TUDCA. TUDCA reconciled obesity-associated decreased in SERCA activity and expression, and increase in serine phosphorylation of IRS, total and phosphorylated cJun, ER stress markers Bip, peIF2α and pPERK. Obesity-induced changes in phospholamban and HSP90 were unaffected by TUDCA. In vitro finding revealed that TUDCA ablated palmitic acid-induced cardiomyocyte contractile dysfunction. In summary, these data depicted a pivotal role of ER stress in obesity-associated cardiac contractile dysfunction, suggesting the therapeutic potential of ER stress as a target in the management of cardiac dysfunction in obesity. PMID:21035453

Acute transient cognitive dysfunction and acute brain injury induced by systemic inflammation occur by dissociable IL-1-dependent mechanisms.

PubMed

Skelly, Donal T; Griffin, Éadaoin W; Murray, Carol L; Harney, Sarah; O'Boyle, Conor; Hennessy, Edel; Dansereau, Marc-Andre; Nazmi, Arshed; Tortorelli, Lucas; Rawlins, J Nicholas; Bannerman, David M; Cunningham, Colm

2018-06-06

Systemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. Episodes of delirium also contribute to rates of long-term cognitive decline, implying that these acute events induce injury. Whether systemic inflammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mechanisms remains unexplored. Here we show that systemic inflammation, induced by bacterial LPS, produces both working-memory deficits and acute brain injury in the degenerating brain and that these occur by dissociable IL-1-dependent processes. In normal C57BL/6 mice, LPS (100 µg/kg) did not affect working memory but impaired long-term memory consoliodation. However prior hippocampal synaptic loss left mice selectively vulnerable to LPS-induced working memory deficits. Systemically administered IL-1 receptor antagonist (IL-1RA) was protective against, and systemic IL-1β replicated, these working memory deficits. Dexamethasone abolished systemic cytokine synthesis and was protective against working memory deficits, without blocking brain IL-1β synthesis. Direct application of IL-1β to ex vivo hippocampal slices induced non-synaptic depolarisation and irrevesible loss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in the degenerating brain, in an IL-1RI -/- -dependent fashion. The data suggest that LPS induces working memory dysfunction via circulating IL-1β but direct hippocampal action of IL-1β causes neuronal dysfunction and may drive neuronal death. The data suggest that acute systemic inflammation produces both reversible cognitive deficits, resembling delirium, and acute brain injury contributing to long-term cognitive impairment but that these events are mechanistically dissociable. These data have significant implications for management of cognitive dysfunction during acute illness.

Hospital collaboration with emergency medical services in the care of patients with acute myocardial infarction: perspectives from key hospital staff.

PubMed

Landman, Adam B; Spatz, Erica S; Cherlin, Emily J; Krumholz, Harlan M; Bradley, Elizabeth H; Curry, Leslie A

2013-02-01

Evidence suggests that active collaboration between hospitals and emergency medical services (EMS) is significantly associated with lower acute myocardial infarction mortality rates; however, the nature of such collaborations is not well understood. We seek to characterize views of key hospital staff about collaboration with EMS in the care of patients hospitalized with acute myocardial infarction. We performed an exploratory analysis of qualitative data previously collected from site visits and detailed interviews with 11 US hospitals that ranked in the top or bottom 5% of performance on 30-day risk-standardized acute myocardial infarction mortality rates, using Centers for Medicare & Medicaid Services data from 2005 to 2007. We selected all codes from the previous analysis in which EMS was most likely to have been discussed. A multidisciplinary team analyzed the data with the constant comparative method to generate recurrent themes. Both higher- and lower-performing hospitals reported that EMS is critical to the provision of timely care for patients with acute myocardial infarction. However, close collaborative relationships with EMS were more apparent in the higher-performing hospitals, which demonstrated specific investment in and attention to EMS through respect for EMS as valued professionals and colleagues, strong communication and coordination with EMS and active engagement of EMS in hospital acute myocardial infarction quality improvement efforts. Hospital staff from higher-performing hospitals described broad, multifaceted strategies to support collaboration with EMS in providing acute myocardial infarction care. The association of these strategies with hospital performance should be tested quantitatively in a larger representative study. Copyright © 2012. Published by Mosby, Inc.

Usefulness of Speckle-Tracking Imaging for Right Ventricular Assessment after Acute Myocardial Infarction: A Magnetic Resonance Imaging/Echocardiographic Comparison within the Relation between Aldosterone and Cardiac Remodeling after Myocardial Infarction Study.

PubMed

Lemarié, Jérémie; Huttin, Olivier; Girerd, Nicolas; Mandry, Damien; Juillière, Yves; Moulin, Frédéric; Lemoine, Simon; Beaumont, Marine; Marie, Pierre-Yves; Selton-Suty, Christine

2015-07-01

Right ventricular (RV) dysfunction after acute myocardial infarction (AMI) is frequent and associated with poor prognosis. The complex anatomy of the right ventricle makes its echocardiographic assessment challenging. Quantification of RV deformation by speckle-tracking echocardiography is a widely available and reproducible technique that readily provides an integrated analysis of all segments of the right ventricle. The aim of this study was to investigate the accuracy of conventional echocardiographic parameters and speckle-tracking echocardiographic strain parameters in assessing RV function after AMI, in comparison with cardiac magnetic resonance imaging (CMR). A total of 135 patients admitted for AMI (73 anterior, 62 inferior) were prospectively studied. Right ventricular function was assessed by echocardiography and CMR within 2 to 4 days of hospital admission. Right ventricular dysfunction was defined as CMR RV ejection fraction < 50%. Right ventricular global peak longitudinal systolic strain (GLPSS) was calculated by averaging the strain values of the septal, lateral, and inferior walls. Right ventricular dysfunction was documented in 20 patients. Right ventricular GLPSS was the best echographic correlate of CMR RV ejection fraction (r = -0.459, P < .0001) and possessed good diagnostic value for RV dysfunction (area under the receiver operating characteristic curve [AUROC], 0.724; 95% CI, 0.590-0.857), which was comparable with that of RV fractional area change (AUROC, 0.756; 95% CI, 0.647-0.866). In patients with inferior myocardial infarctions, the AUROCs for RV GLPSS (0.822) and inferolateral strain (0.877) were greater than that observed for RV fractional area change (0.760) Other conventional echocardiographic parameters performed poorly (all AUROCs < 0.700). After AMI, RV GLPSS is the best correlate of CMR RV ejection fraction. In patients with inferior AMIs, RV GLPSS displays even higher diagnostic value than conventional echocardiographic

In vivo determination of acute myocardial ischemia based on photoacoustic imaging with a focused transducer

NASA Astrophysics Data System (ADS)

Li, Zhifang; Li, Hui; Chen, Haiyu; Xie, Wengming

2011-07-01

The location and ischemia extent are two important parameters for evaluating the acute myocardial ischemia (AMI). A focused-transducer-based photoacoustic imaging method was employed to assess time-dependent AMI. Our preliminary results show that the photoacoustic signal could identify the myocardium. The intensity and area of photoacoustic images of myocardium could be used for characterizing the ischemia extent and scope of myocardial ischemia. The results also imply that the intensity and area of photoacoustic images are the rapid fall of an exponential model with an increase of delaying time after the left anterior descending coronary artery (LAD) occlusion. These experimental results were consistent with the clinical characteristics. The findings suggest that the photoacoustic imaging be a potential tool for the real-time assessment of acute myocardial ischemia during surgical operation.

Transarterial pacemaker lead implantation results in acute myocardial infarction.

PubMed

Issa, Ziad F; Gill, John B

2010-11-01

We report a case of inadvertent transarterial implantation of dual-chamber pacemaker leads; the ventricular lead positioned across the aortic valve into the left ventricle and the atrial lead curving in the aortic root with the tip positioned into the left circumflex artery, resulting in acute myocardial infarction. The diagnosis was made based on the finding on the chest X-ray, surface ECG, and coronary angiography.

Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone

PubMed Central

Shimkunas, Rafael; Makwana, Om; Spaulding, Kimberly; Bazargan, Mona; Khazalpour, Michael; Takaba, Kiyoaki; Soleimani, Mehrdad; Myagmar, Bat-Erdene; Lovett, David H.; Simpson, Paul C.; Ratcliffe, Mark B.

2014-01-01

After myocardial infarction, a poorly contracting nonischemic border zone forms adjacent to the infarct. The cause of border zone dysfunction is unclear. The goal of this study was to determine the myofilament mechanisms involved in postinfarction border zone dysfunction. Two weeks after anteroapical infarction of sheep hearts, we studied in vitro isometric and isotonic contractions of demembranated myocardium from the infarct border zone and a zone remote from the infarct. Maximal force development (Fmax) of the border zone myocardium was reduced by 31 ± 2% versus the remote zone myocardium (n = 6/group, P < 0.0001). Decreased border zone Fmax was not due to a reduced content of contractile material, as assessed histologically, and from myosin content. Furthermore, decreased border zone Fmax did not involve altered cross-bridge kinetics, as assessed by muscle shortening velocity and force development kinetics. Decreased border zone Fmax was associated with decreased cross-bridge formation, as assessed from muscle stiffness in the absence of ATP where cross-bridge formation should be maximized (rigor stiffness was reduced 34 ± 6%, n = 5, P = 0.011 vs. the remote zone). Furthermore, the border zone myocardium had significantly reduced phosphorylation of myosin essential light chain (ELC; 41 ± 10%, n = 4, P < 0.05). However, for animals treated with doxycycline, an inhibitor of matrix metalloproteinases, rigor stiffness and ELC phosphorylation were not reduced in the border zone myocardium, suggesting that doxycycline had a protective effect. In conclusion, myofilament dysfunction contributes to postinfarction border zone dysfunction, myofilament dysfunction involves impaired cross-bridge formation and decreased ELC phosphorylation, and matrix metalloproteinase inhibition may be beneficial for limiting postinfarct border zone dysfunction. PMID:25128171

Prefrontal Cortex Corticotropin-Releasing Factor Receptor 1 Conveys Acute Stress-Induced Executive Dysfunction.

PubMed

Uribe-Mariño, Andrés; Gassen, Nils C; Wiesbeck, Maximilian F; Balsevich, Georgia; Santarelli, Sara; Solfrank, Beate; Dournes, Carine; Fries, Gabriel R; Masana, Merce; Labermeier, Christiana; Wang, Xiao-Dong; Hafner, Kathrin; Schmid, Bianca; Rein, Theo; Chen, Alon; Deussing, Jan M; Schmidt, Mathias V

2016-11-15

The medial prefrontal cortex (mPFC) subserves complex cognition and is impaired by stress. Corticotropin-releasing factor (CRF), through CRF receptor 1 (CRFR1), constitutes a key element of the stress response. However, its contribution to the effects of stress in the mPFC remains unclear. Mice were exposed to acute social defeat stress and subsequently to either the temporal order memory (n = 11-12) or reversal learning (n = 9-11) behavioral test. Changes in mPFC Crhr1 messenger RNA levels were measured in acutely stressed mice (n = 12). Crhr1 loxP/loxP mice received either intra-mPFC adeno-associated virus-Cre or empty microinjections (n = 17-20) and then were submitted to acute stress and later to the behavioral tests. Co-immunoprecipitation was used to detect activation of the protein kinase A (PKA) signaling pathway in the mPFC of acutely stressed mice (n = 8) or intra-mPFC CRF injected mice (n = 7). Finally, mice received intra-mPFC CRF (n = 11) and/or Rp-isomer cyclic adenosine 3',5' monophosphorothioate (Rp-cAMPS) (n = 12) microinjections and underwent behavioral testing. We report acute stress-induced effects on mPFC-mediated cognition, identify CRF-CRFR1-containing microcircuits within the mPFC, and demonstrate stress-induced changes in Crhr1 messenger RNA expression. Importantly, intra-mPFC CRFR1 deletion abolishes acute stress-induced executive dysfunction, whereas intra-mPFC CRF mimics acute stress-induced mPFC dysfunction. Acute stress and intra-mPFC CRF activate the PKA signaling pathway in the mPFC, leading to cyclic AMP response element binding protein phosphorylation in intra-mPFC CRFR1-expressing neurons. Finally, PKA blockade reverses the intra-mPFC CRF-induced executive dysfunction. Taken together, these results unravel a molecular mechanism linking acute stress to executive dysfunction via CRFR1. This will aid in the development of novel therapeutic targets for stress-induced cognitive dysfunction. Copyright © 2016 Society of Biological

Early organ-specific mitochondrial dysfunction of jejunum and lung found in rats with experimental acute pancreatitis

PubMed Central

Mittal, Anubhav; Hickey, Anthony JR; Chai, Chau C; Loveday, Benjamin PT; Thompson, Nichola; Dare, Anna; Delahunt, Brett; Cooper, Garth JS; Windsor, John A; Phillips, Anthony RJ

2011-01-01

Introduction Multiple organ dysfunction is the main cause of death in severe acute pancreatitis. Primary mitochondrial dysfunction plays a central role in the development and progression of organ failure in critical illness. The present study investigated mitochondrial function in seven tissues during early experimental acute pancreatitis. Methods Twenty-eight male Wistar rats (463 ± 2 g; mean ± SEM) were studied. Group 1 (n = 8), saline control; Group 2 (n = 6), caerulein-induced mild acute pancreatitis; Group 3 (n = 7) sham surgical controls; and Group 4 (n = 7), taurocholate-induced severe acute pancreatitis. Animals were euthanased at 6 h from the induction of acute pancreatitis and mitochondrial function was assessed in the heart, lung, liver, kidney, pancreas, duodenum and jejunum by mitochondrial respirometry. Results Significant early mitochondrial dysfunction was present in the pancreas, lung and jejunum in both models of acute pancreatitis, however, the Heart, liver, kidney and duodenal mitochondria were unaffected. Conclusions The present study provides the first description of early organ-selective mitochondrial dysfunction in the lung and jejunum during acute pancreatitis. Research is now needed to identify the underlying pathophysiology behind the organ selective mitochondrial dysfunction, and the potential benefits of early mitochondrial-specific therapies in acute pancreatitis. PMID:21492333

Proteinuria and Reduced Estimated Glomerular Filtration Rate Independently Predict Risk for Acute Myocardial Infarction: Findings from a Population-Based Study in Keelung, Taiwan.

PubMed

Chang, Shu-Hsuan; Tsai, Chia-Ti; Yen, Amy Ming-Fang; Lei, Meng-Huan; Chen, Hsiu-Hsi; Tseng, Chuen-Den

2015-03-01

The aim of this study was to evaluate the independent roles of proteinuria and reduced estimated glomerular filtration rate (GFR) in the development of acute myocardial infarction in a northern Taiwanese population. We conducted a community-based prospective cohort study in Keelung, the northernmost county of Taiwan. A total of 63,129 subjects (63% women) ≥ 20 years of age who had no history of coronary heart disease were recruited and followed-up. Univariate and multivariate proportional hazards regression analysis was performed to assess the association between proteinuria and estimated GFR and the risk of acute myocardial infarction. There were 305 new cases of acute myocardial infarction (114 women and 191 men) documented during a four-year follow-up period. After adjustment of potential confounding covariates, heavier proteinuria (dipstick urinalysis reading 3+) and estimated GFR of less than 60 ml/min/1.73 m(2) independently predicted increased risk of developing acute myocardial infarction. The adjusted hazard ratio (aHR) of heavier proteinuria for occurrence of acute myocardial infarction was 1.85 [95% confidence intervals (CI), 1.17-2.91, p < 0.01] (vs. the reference group: negative dipstick proteinuria). The aHR of estimated GFR of 30-59 ml/min/1.73 m(2) for occurrence of acute myocardial infarction was 2.4 (95% CI, 1.31-4.38, p < 0.01) (vs. the reference group: estimated GFR ≥ 90 ml/ min/1.73 m(2)), and that of estimated GFR of 15-29 ml/min/1.73 m(2) was 5.26 (95% CI, 2.26-12.26, p < 0.01). We demonstrated that both heavier proteinuria and lower estimated GFR are significant independent predictors of developing future acute myocardial infarction in a northern Taiwanese population. Acute myocardial infarction; Estimated glomerular filtration rate; Proteinuria.

Illness representation after acute myocardial infarction: impact on in-hospital recovery.

PubMed

Cherrington, Candace C; Moser, Debra K; Lennie, Terry A; Kennedy, Carol W

2004-03-01

Despite significant progress in the treatment of coronary artery disease, myocardial infarction is still the leading cause of death in the United States. As suggested by Leventhal's Self-Regulation Model of Illness, the continued high morbidity and mortality may be due to a failure to address the role of psychosocial factors such as illness representation, depression, and anxiety in recovery. To determine the relationship between illness representation of myocardial infarction and the occurrence of in-hospital complications and if anxiety and depression mediate this relationship. A prospective correlational design was used to measure illness representation, depression, and anxiety 24 to 48 hours after admission for myocardial infarction in 49 patients and the frequency of complications during the acute event. Logistic regression was used to determine the likelihood of experiencing a complication. When demographic and clinical variables were controlled for, the more negative the representation of illness, the greater were the odds of experiencing a complication (chi2 = 16.9, df = 6, P =.01). The odds of experiencing a complication increased 5.1% for each 1 unit increase in the score on the Illness Preparation Questionnaire (B = 0.05, Wald = 4.442, Exp(B) = 1.051, 95% CI = 1.003-1.1010). Neither anxiety (chi2 = 3.0, df = 1, P =. 09) nor depression (chi2 = 2.5, df = 1, P = .11) were significant predictors of the occurrence of complications. In these patients, illness representation was predictive of the likelihood of experiencing a complication. Thus, illness representation appears to be an important psychosocial factor in acute recovery from myocardial infarction.

Levels of platelet-derived microparticles and soluble p-selectin in patients of acute myocardial infarction (case control study).

PubMed

Hameed, Aisha; Rubab, Zille; Abbas Rizvi, Syed Khizar; Hussain, Shabbir; Latif, Waqas; Mohsin, Shahida

2017-07-01

TTo measure levels of platelet-derived microparticles and soluble P-selectin in patients of acute myocardial infarction and their comparison with healthy controls. This case-control study was conducted in Department of Haematology, University of Health Sciences Lahore from April to September 2013, and comprised patients of acute myocardial infarction in group 1 and healthy controls in group 2. Platelet-derived microparticles and soluble P-selectin were measured by enzyme-linked immunosorbent assay. SPSS21 was used for data analysis. Of the 80 participants, 50(62.5%) were patients and 30(37.5%) were controls. The mean levels of platelet-derived microparticles and soluble P-selectin were significantly higher in group 1 compared to group 2 (45.70±10.30 vs 10.60±0.96, and 51.46±9.30 vs 9.16±1.04, respectively) (p<0.001). There was no significant difference in levels of platelet-derived microparticles and soluble P-selectin in three intervals after acute myocardial infarction (p>0.05). Although levels of platelet-derived microparticles and soluble P-selectin did not correlate to creatinekinase-myocardial band levels (p>0.05), but there was a trend of significant correlation with cardiac troponin T (p<0.05). Levels of platelet-derived microparticles and soluble P-selectin can be used as novel early diagnostic marker of acute myocardial infarction.

Thrombolytic therapy use for acute myocardial infarction and outcome in Qatar.

PubMed

Hadi, Hadi A R; Al Suwaidi, J; Bener, A; Khinji, A; Al Binali, H A

2005-07-10

Data on the outcome of patients treated with thrombolytic therapy in the Arab world is scarce. The main objective of this study is to study the 7-day morbidity and mortality rate and the rate of use of thrombolytic therapy in patients presenting with acute myocardial infarction treated with thrombolytic therapy in the Middle East. We conducted a retrospective analysis of prospectively collected data for all patients who were admitted to Coronary Care Unit in Cardiology Department in Hamad Medical during the period (1991-2001). Patients were divided into two groups in relation to ethnicity whether they received thrombolysis or not. In each group, the number of patients, age at the time of admission, gender, cardiovascular risk profile, therapy and outcome in regard of in-hospital complication and 7-day death as primary end point were analyzed. Of the total 5388 patients admitted with acute myocardial infarction during the 10-year period, 66.3% (3567) with STE MI were found, 61.4% (2190) of them received thrombolytic therapy while 38.6% (1377) were not eligible for thrombolytic therapy. The remaining 33.7% (1821) were admitted with non-STE MI. In consideration of ethnic variation, patients with STE MI eligible for thrombolytic therapy, 29.6% (1598) were Qataris and 70.4% (3792) were non-Qataris. Thrombolytic therapy was administered to 25.9% (414) of Qatari patients and 51.3% (1947) of non-Qataris. The mortality rate of Qatari patients who received thrombolytic therapy was 9.2% (38) vs. 19.5% (231) who did not receive thrombolytic therapy (p<0.001). In non-Qatari patients, the mortality rate was 5.2% (102) for those who received thrombolytic therapy, while it was 8.6% (159) for those with no thrombolytic therapy (p<0.001). When compared to male patients, female patients with thrombolytic therapy had higher mortality rates (in both Qataris and non-Qataris) (20.5% vs. 6.1%; p value<0.001 and 16.1% vs. 9.4%; p<0.001, respectively), there were no significant differences

[Myocardial ultrastructural changes in rats following different levels of acute +Gz exposure].

PubMed

Zheng, Jun; Liu, Cheng-gang; Ren, Li; Xiao, Xiao-guang; Xu, Shu-xuan; Wang, Ping; Ji, Gui-ying

2004-06-01

To observe the effects of different levels of acute +Gz exposure on myocardial ultrastructure of rats and provide experimental basis for further development of anti-G measures. Twenty male Wistar rats were randomly divided into 4 groups (n=5): normal control group, +20 Gz group, +10 Gz group and +5 Gz group. Profile of the centrifuge +Gz exposure was trapezoidal, in which +20 Gz lasted for 30 s, +10 Gz for 1.5 min. +5 Gz exposure was repeated for 3 times with 30 min interval and each for 1.5 min. Myocardial tissue of left ventricle was sampled for transmission electron microscopy 5 h after exposure. +20 Gz and +10 Gz exposure caused obvious edema of myocardial and endothelial cells, myofibril disorder and injuries of mitochondria and nucleus. Breaks of myocardial fiber, formation of contraction bands and rupture of mitochondria were also observed in +20 Gz group. In +5 Gz group, there was still slight edema of myocardial and endothelial cells, while organic changes of myocardial ultrastructure were not observed. High +Gz exposure can cause myocardial ultrastructural injury in rats. Slight reversible injured response can also be observed in myocardial cell after repeated moderate level of +Gz exposure. This indicates that attention should be paid to the study of the effect of high +Gz on heart in pilots.

Cells involved in extracellular matrix remodeling after acute myocardial infarction

PubMed Central

Garcia, Larissa Ferraz; Mataveli, Fábio D’Aguiar; Mader, Ana Maria Amaral Antônio; Theodoro, Thérèse Rachell; Justo, Giselle Zenker; Pinhal, Maria Aparecida da Silva

2015-01-01

Objective Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Methods Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. Results There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation. Conclusion The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct. PMID:25993074

Evaluation of mechanical dyssynchrony and myocardial perfusion using phase analysis of gated SPECT imaging in patients with left ventricular dysfunction

PubMed Central

Trimble, Mark A.; Borges-Neto, Salvador; Honeycutt, Emily F.; Shaw, Linda K.; Pagnanelli, Robert; Chen, Ji; Iskandrian, Ami E.; Garcia, Ernest V.; Velazquez, Eric J.

2010-01-01

Background Using phase analysis of gated single photon emission computed tomography (SPECT) imaging, we examined the relation between myocardial perfusion, degree of electrical dyssynchrony, and degree of SPECT-derived mechanical dyssynchrony in patients with left ventricular (LV) dysfunction. Methods and Results We retrospectively examined 125 patients with LV dysfunction and ejection fraction of 35% or lower. Fourier analysis converts regional myocardial counts into a continuous thickening function, allowing resolution of phase of onset of myocardial thickening. The SD of LV phase distribution (phase SD) and histogram bandwidth describe LV phase dispersion as a measure of dyssynchrony. Heart failure (HF) patients with perfusion abnormalities ities have higher degrees of dyssynchrony measured by median phase SD (45.5° vs 27.7°, P < .0001) and bandwidth (117.0° vs 73.0°, P = .0006). HF patients with prolonged QRS durations have higher degrees of dyssynchrony measured by median phase SD (54.1° vs 34.7°, P < .0001) and bandwidth (136.5° vs 99.0°, P = .0005). Mild to moderate correlations exist between QRS duration and phase analysis indices of phase SD (r = 0.50) and bandwidth (r = 0.40). Mechanical dyssynchrony (phase SD >43°) was 43.2%. Conclusions HF patients with perfusion abnormalities or prolonged QRS durations QRS durations have higher degrees of mechanical dyssynchrony. Gated SPECT myocardial perfusion imaging can quantify myocardial function, perfusion, and dyssynchrony and may help in evaluating patients for cardiac resynchronization therapy. PMID:18761269

The effects of compound danshen dripping pills and human umbilical cord blood mononuclear cell transplant after acute myocardial infarction.

PubMed

Jun, Yi; Chunju, Yuan; Qi, Ai; Liuxia, Deng; Guolong, Yu

2014-04-01

The low frequency of survival of stem cells implanted in the myocardium after acute myocardial infarction may be caused by inflammation and oxidative stress in the myocardial microenvironment. We evaluated the effects of a traditional Chinese medicine, Compound Danshen Dripping Pills, on the cardiac microenvironment and cardiac function when used alone or in combination with human umbilical cord blood mononuclear cell transplant after acute myocardial infarction. After surgically induced acute myocardial infarction, rabbits were treated with Compound Danshen Dripping Pills alone or in combination with human umbilical cord blood mononuclear cell transplant. Evaluation included histology, measurement of left ventricular ejection fraction and fractional shortening, leukocyte count, count of green fluorescent protein positive cells, superoxide dismutase activity, and malondialdehyde content. Combination treatment with Compound Danshen Dripping Pills and human umbilical cord blood mononuclear cell transplant significantly increased the survival of implanted cells, inhibited cardiac cell apoptosis, decreased oxidative stress, decreased the inflammatory response, and improved cardiac function. Rabbits treated with either Compound Danshen Dripping Pills or human umbilical cord blood mononuclear cells alone had improvement in these effects compared with untreated control rabbits. Combination therapy with Compound Danshen Dripping Pills and human umbilical cord blood mononuclear cells may improve cardiac function and morphology after acute myocardial infarction.

Prospective evaluation of eligibility for thrombolytic therapy in acute myocardial infarction.

PubMed Central

French, J. K.; Williams, B. F.; Hart, H. H.; Wyatt, S.; Poole, J. E.; Ingram, C.; Ellis, C. J.; Williams, M. G.; White, H. D.

1996-01-01

OBJECTIVES--To determine the proportion of patients presenting with acute myocardial infarction who are eligible for thrombolytic therapy. DESIGN--Cohort follow up study. SETTING--The four coronary care units in Auckland, New Zealand. SUBJECTS--All 3014 patients presenting to the units with suspected myocardial infarction in 1993. MAIN OUTCOME MEASURES--Eligibility for reperfusion with thrombolytic therapy (presentation within 12 hours of the onset of ischaemic chest pain with ST elevation > or = 2 mm in leads V1-V3, ST elevation > or = 1 mm in any other two contiguous leads, or new left bundle branch block); proportions of (a) patients eligible for reperfusion and (b) patients with contraindications to thrombolysis; death (including causes); definite myocardial infarction. RESULTS--948 patients had definite myocardial infarction, 124 probable myocardial infarction, and nine ST elevation but no infarction; 1274 patients had unstable angina and 659 chest pain of other causes. Of patients with definite or probable myocardial infarction, 576 (53.3%) were eligible for reperfusion, 39 had definite contraindications to thrombolysis (risk of bleeding). Hence 49.7% of patients (537/1081) were eligible for thrombolysis and 43.5% (470) received this treatment. Hospital mortality among patients eligible for reperfusion was 11.7% (55/470 cases) among those who received thrombolysis and 17.0% (18/106) among those who did not. CONCLUSIONS--On current criteria about half of patients admitted to coronary care units with definite or probable myocardial infarction are eligible for thrombolytic therapy. Few eligible patients have definite contraindications to thrombolytic therapy. Mortality for all community admissions for myocardial infarction remains high. PMID:8664716

Stimulation of ganglionated plexus attenuates cardiac neural remodeling and heart failure progression in a canine model of acute heart failure post-myocardial infarction.

PubMed

Luo, Da; Hu, Huihui; Qin, Zhiliang; Liu, Shan; Yu, Xiaomei; Ma, Ruisong; He, Wenbo; Xie, Jing; Lu, Zhibing; He, Bo; Jiang, Hong

2017-12-01

Heart failure (HF) is associated with autonomic dysfunction. Vagus nerve stimulation has been shown to improve cardiac function both in HF patients and animal models of HF. The purpose of this present study is to investigate the effects of ganglionated plexus stimulation (GPS) on HF progression and autonomic remodeling in a canine model of acute HF post-myocardial infarction. Eighteen adult mongrel male dogs were randomized into the control (n=8) and GPS (n=10) groups. All dogs underwent left anterior descending artery ligation followed by 6-hour high-rate (180-220bpm) ventricular pacing to induce acute HF. Transthoracic 2-dimensional echocardiography was performed at different time points. The plasma levels of norepinephrine, B-type natriuretic peptide (BNP) and Ang-II were measured using ELISA kits. C-fos and nerve growth factor (NGF) proteins expressed in the left stellate ganglion as well as GAP43 and TH proteins expressed in the peri-infarct zone were measured using western blot. After 6h of GPS, the left ventricular end-diastolic volume, end-systolic volume and ejection fraction showed no significant differences between the 2 groups, but the interventricular septal thickness at end-systole in the GPS group was significantly higher than that in the control group. The plasma levels of norepinephrine, BNP, Ang-II were increased 1h after myocardial infarction while the increase was attenuated by GPS. The expression of c-fos and NGF proteins in the left stellate ganglion as well as GAP43 and TH proteins in cardiac peri-infarct zone in GPS group were significantly lower than that in control group. GPS inhibits cardiac sympathetic remodeling and attenuates HF progression in canines with acute HF induced by myocardial infarction and ventricular pacing. Copyright © 2017 Elsevier B.V. All rights reserved.

[Comparison of initial and delayed myocardial imaging with beta-methyl-p-[123I]-iodophenylpentadecanoic acid in acute myocardial infarction].

PubMed

Naruse, H; Yoshimura, N; Yamamoto, J; Morita, M; Fukutake, N; Ohyanagi, M; Iwasaki, T; Fukuchi, M

1994-01-01

Myocardial imaging using beta-methyl-p-[123I]-iodophenylpentadecanoic acid (BMIPP) of 15 patients with acute myocardial infarction was performed to assess "fill-in" and "washout" defects in the delayed myocardial image. The initial and delayed images were evaluated by a visual and quantitative washout rate method. Visual judgement found 8/180 (4%) segments showed "fill-in" defects, and 24/180 segments (13%) showed "washout" defects. There was no relationship between days from onset to the study and the frequency of fill-in and washout defects. The mean washout rate in the segments with "fill-in" defects was 9.0 +/- 16.6%, and that of "washout" defects was 24.9 +/- 18.1% which was significantly higher than in controls (8.7 +/- 15.4%, p < 0.05). There was no correlation between mean washout rate and total blood lipids, total cholesterol, triglyceride and HDL-cholesterol. Therefore, neither time from onset nor blood lipids level was related to changes from the initial image to the delayed image. These changes may be due to relative (false) findings due to changes in circumference, and may be based on myocardial characteristics after myocardial infarction and/or reperfusion.

Diagnostic Accuracy of a New High-Sensitivity Troponin I Assay and Five Accelerated Diagnostic Pathways for Ruling Out Acute Myocardial Infarction and Acute Coronary Syndrome.

PubMed

Greenslade, Jaimi H; Carlton, Edward W; Van Hise, Christopher; Cho, Elizabeth; Hawkins, Tracey; Parsonage, William A; Tate, Jillian; Ungerer, Jacobus; Cullen, Louise

2018-04-01

This diagnostic accuracy study describes the performance of 5 accelerated chest pain pathways, calculated with the new Beckman's Access high-sensitivity troponin I assay. High-sensitivity troponin I was measured with presentation and 2-hour blood samples in 1,811 patients who presented to an emergency department (ED) in Australia. Patients were classified as being at low risk according to 5 rules: modified accelerated diagnostic protocol to assess patients with chest pain symptoms using troponin as the only biomarker (m-ADAPT), the Emergency Department Assessment of Chest Pain Score (EDACS) pathway, the History, ECG, Age, Risk Factors, and Troponin (HEART) pathway, the No Objective Testing Rule, and the new Vancouver Chest Pain Rule. Endpoints were 30-day acute myocardial infarction and acute coronary syndrome. Measures of diagnostic accuracy for each rule were calculated. Data included 96 patients (5.3%) with acute myocardial infarction and 139 (7.7%) with acute coronary syndrome. The new Vancouver Chest Pain Rule and No Objective Testing Rule had high sensitivity for acute myocardial infarction (100%; 95% confidence interval [CI] 96.2% to 100% for both) and acute coronary syndrome (98.6% [95% CI 94.9% to 99.8%] and 99.3% [95% CI 96.1% to 100%]). The m-ADAPT, EDACS, and HEART pathways also yielded high sensitivity for acute myocardial infarction (96.9% [95% CI 91.1% to 99.4%] for m-ADAPT and 97.9% [95% CI 92.7% to 99.7%] for EDACS and HEART), but lower sensitivity for acute coronary syndrome (≤95.0% for all). The m-ADAPT, EDACS, and HEART rules classified more patients as being at low risk (64.3%, 62.5%, and 49.8%, respectively) than the new Vancouver Chest Pain Rule and No Objective Testing Rule (28.2% and 34.5%, respectively). In this cohort with a low prevalence of acute myocardial infarction and acute coronary syndrome, using the Beckman's Access high-sensitivity troponin I assay with the new Vancouver Chest Pain Rule or No Objective Testing Rule enabled

Right ventricular dysfunction in acute pulmonary embolism: NT-proBNP vs. troponin T.

PubMed

Cotugno, Marilena; Orgaz-Molina, Jacinto; Rosa-Salazar, Vladimir; Guirado-Torrecillas, Leticia; García-Pérez, Bartolomé

2017-04-21

Dysfunction of the right ventricle (RV) is a parameter of severity in acute pulmonary embolism (PE). Echocardiographic assessment is not always possible in accident and emergency, hence the need to predict the presence of RV dysfunction using easily measurable parameters. To analyse the value of NT-proBNP and troponin T as markers of RV dysfunction in patients with acute PE. Secondarily, to assess the relationship between RV failure and clinical parameters related to PE. Analytical, observational, cross-sectional and retrospective study comparing the values NT-proBNP, troponin T and presenting symptoms of PE among patients with and without RV dysfunction. One hundred seventy-two patients (52 with RV failure,120 without) were included. All symptoms occurred with similar frequency between the 2groups except dyspnea and syncope (more common in the group with RV failure). Both NT-proBNP and troponin T had significantly higher values in the group of patients with RV dysfunction. However, in the multivariate analysis, NT-proBNP had a higher explanatory value for RV failure than troponin T. NT-proBNP is a diagnostic parameter of RV dysfunction with higher sensitivity in the context of acute PE. Copyright © 2016 Elsevier España, S.L.U. All rights reserved.

Detection of periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction.

PubMed

Ohki, Takahiro; Itabashi, Yuji; Kohno, Takashi; Yoshizawa, Akihiro; Nishikubo, Shuichi; Watanabe, Shinya; Yamane, Genyuki; Ishihara, Kazuyuki

2012-02-01

Numerous reports have demonstrated that periodontal bacteria are present in plaques from atherosclerotic arteries. Although periodontitis has recently been recognized as a risk factor for coronary artery disease, the direct relationship between periodontal bacteria and coronary artery disease has not yet been clarified. It has been suggested that these bacteria might contribute to inflammation and plaque instability. We assumed that if periodontal bacteria induce inflammation of plaque, the bacteria would be released into the bloodstream when vulnerable plaque ruptures. To determine whether periodontal bacteria are present in thrombi at the site of acute myocardial infarction, we tried to detect periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction (PCR). We studied 81 consecutive adults with ST-segment elevation acute myocardial infarction who underwent primary percutaneous coronary intervention (PCI). All patients underwent removal of thrombus with aspiration catheters at the beginning of percutaneous coronary intervention, and a small sample of thrombus was obtained for PCR. The detection rates of periodontal bacteria by PCR were 19.7% for Aggregatibacter actinomycetemcomitans, 3.4% for Porphyromonas gingivalis, and 2.3% for Treponema denticola. Three species of periodontal bacteria were detected in the thrombi of patients with acute myocardial infarction. This raises the possibility that such bacteria are latently present in plaque and also suggests that these bacteria might have a role in plaque inflammation and instability. Copyright © 2012 Mosby, Inc. All rights reserved.

[Surgical cryoablation and left ventriculoplasty for electrical storm after acute myocardial infarction].

PubMed

Tobe, Satoshi; Yoshida, K; Adachi, K; Fukase, K; Tanimura, N; Yamaguchi, M

2008-03-01

A 65-year-old man was referred to our hospital to treat recent anterior myocardial infarction. Coronary artery angiography showed acute occlusion of left anterior descending coronary artery (LAD) and chronic occlusion of right coronary artery. After emergent percutaneous coronary intervention for LAD, drug-refractory electrical storm necessitating frequent electrical defibrillating cardioversion occurred. This patient successfully underwent surgical cryoablation, left ventriculoplasty and coronary revascularization. At 2 years and 10th month after the operation, he is well without limitation of daily activities and any evidence of myocardial ischemia and ventricular tachycardia.

Decreased Autophagy Contributes to Myocardial Dysfunction in Rats Subjected to Nonlethal Mechanical Trauma

PubMed Central

Liang, Feng; Li, Xiaoyu; Wang, Li; Yang, Caihong; Yan, Zi; Zhang, Suli; Liu, Huirong

2013-01-01

Autophagy is important in cells for removing damaged organelles, such as mitochondria. Insufficient autophagy plays a critical role in tissue injury and organ dysfunction under a variety of pathological conditions. However, the role of autophagy in nonlethal traumatic cardiac damage remains unclear. The aims of the present study were to investigate whether nonlethal mechanical trauma may result in the change of cardiomyocyte autophagy, and if so, to determine whether the changed myocardial autophagy may contribute to delayed cardiac dysfunction. Male adult rats were subjected to nonlethal traumatic injury, and cardiomyocyte autophagy, cardiac mitochondrial function, and cardiac function in isolated perfused hearts were detected. Direct mechanical traumatic injury was not observed in the heart within 24 h after trauma. However, cardiomyocyte autophagy gradually decreased and reached a minimal level 6 h after trauma. Cardiac mitochondrial dysfunction was observed by cardiac radionuclide imaging 6 h after trauma, and cardiac dysfunction was observed 24 h after trauma in the isolated perfused heart. These were reversed when autophagy was induced by administration of the autophagy inducer rapamycin 30 min before trauma. Our present study demonstrated for the first time that nonlethal traumatic injury caused decreased autophagy, and decreased autophagy may contribute to post-traumatic organ dysfunction. Though our study has some limitations, it strongly suggests that cardiac damage induced by nonlethal mechanical trauma can be detected by noninvasive radionuclide imaging, and induction of autophagy may be a novel strategy for reducing posttrauma multiple organ failure. PMID:23977036

Hot shot induction and reperfusion with a specific blocker of the es-ENT1 nucleoside transporter before and after hypothermic cardioplegia abolishes myocardial stunning in acutely ischemic hearts despite metabolic derangement: Hot shot drug delivery before hypothermic cardioplegia

PubMed Central

Abd-Elfattah, Anwar Saad; Tuchy, Gert E.; Jessen, Michael E.; Salter, David R.; Goldstein, Jacques P.; Brunsting, Louis A.; Wechsler, Andrew S.

2013-01-01

Objective Simultaneous inhibition of the cardiac equilibrative-p-nitrobenzylthioinosine (NBMPR)–sensitive (es) type of the equilibrative nucleoside transport 1 (ENT1) nucleoside transporter, with NBMPR, and adenosine deaminase, with erythro-9-[2-hydroxy-3-nonyl]adenine (EHNA), prevents release of myocardial purines and attenuates myocardial stunning and fibrillation in canine models of warm ischemia and reperfusion. It is not known whether prolonged administration of hypothermic cardioplegia influences purine release and EHNA/NBMPR-mediated cardioprotection in acutely ischemic hearts. Methods Anesthetized dogs (n = 46), which underwent normothermic aortic crossclamping for 20 minutes on-pump, were divided to determine (1) purine release with induction of intermittent antegrade or continuous retrograde hypothermic cardioplegia and reperfusion, (2) the effects of postischemic treatment with 100 µM EHNA and 25 µM NBMPR on purine release and global functional recovery, and (3) whether a hot shot and reperfusion with EHNA/NBMPR inhibits purine release and attenuates ventricular dysfunction of ischemic hearts. Myocardial biopsies and coronary sinus effluents were obtained and analyzed using high-performance liquid chromatography. Results Warm ischemia depleted myocardial adenosine triphosphate and elevated purines (ie, inosine > adenosine) as markers of ischemia. Induction of intermittent antegrade or continuous retrograde hypothermic (4°C) cardioplegia releases purines until the heart becomes cold (<20°C). During reperfusion, the levels of hypoxanthine and xanthine (free radical substrates) were >90% of purines in coronary sinus effluent. Reperfusion with EHNA/NBMPR abolished ventricular dysfunction in acutely ischemic hearts with and without a hot shot and hypothermic cardioplegic arrest. Conclusions Induction of hypothermic cardioplegia releases purines from ischemic hearts until they become cold, whereas reperfusion induces massive purine release and myocardial

Systemic inflammation is associated with myocardial fibrosis, diastolic dysfunction, and cardiac hypertrophy in patients with hypertrophic cardiomyopathy

PubMed Central

Fang, Lu; Ellims, Andris H; Beale, Anna L; Taylor, Andrew J; Murphy, Andrew; Dart, Anthony M

2017-01-01

Background: Regional or diffuse fibrosis is an early feature of hypertrophic cardiomyopathy (HCM) and is related to poor prognosis. Previous studies have documented low-grade inflammation in HCM. The aim of this study was to examine the relationships between circulating inflammatory markers and myocardial fibrosis, systolic and diastolic dysfunction, and the degree of cardiac hypertrophy in HCM patients. Methods and results: Fifty HCM patients were recruited while 20 healthy subjects served as the control group. Seventeen inflammatory cytokines/chemokines were measured in plasma. Cardiac magnetic resonance imaging and echocardiography were used to assess cardiac phenotypes. Tumour necrosis factor (TNF)-α, interleukin (IL)-6 and serum amyloid P (SAP) were significantly increased in HCM patients compared to controls. IL-6, IL-4, and monocyte chemotactic protein (MCP)-1 were correlated with regional fibrosis while stromal cell-derived factor-1 and MCP-1 were correlated with diffuse fibrosis. Fractalkine and interferon-γ were associated with left ventricular wall thickness. The above associations remained significant in a linear regression model including age, gender, body mass index and family history. TNF-α, IL-6, SAP, MCP-1 and IL-10 were associated with parameters of diastolic dysfunction. White blood cells were also increased in HCM patients and correlated with diffuse fibrosis and diastolic dysfunction. However the associations between parameters of systemic inflammation and diastolic dysfunction were weakened in the linear regression analysis. Conclusions: Systemic inflammation is associated with parameters of the disease severity of HCM patients, particularly regional and diffuse fibrosis. Modifying inflammation may reduce myocardial fibrosis in HCM patients. PMID:29218105

Confluence of depression and acute psychological stress among patients with stable coronary heart disease: effects on myocardial perfusion.

PubMed

Burg, Matthew M; Meadows, Judith; Shimbo, Daichi; Davidson, Karina W; Schwartz, Joseph E; Soufer, Robert

2014-10-30

Depression is prevalent in coronary heart disease (CHD) patients and increases risk for acute coronary syndrome (ACS) recurrence and mortality despite optimal medical care. The pathways underlying this risk remain elusive. Psychological stress (PS) can provoke impairment in myocardial perfusion and trigger ACS. A confluence of acute PS with depression might reveal coronary vascular mechanisms of risk. We tested whether depression increased risk for impaired myocardial perfusion during acute PS among patients with stable CHD. Patients (N=146) completed the Beck Depression Inventory-I (BDI-I), a measure of depression linked to recurrent ACS and post-ACS mortality, and underwent single-photon emission computed tomography myocardial perfusion imaging at rest and during acute PS. The likelihood of new/worsening impairment in myocardial perfusion from baseline to PS as a function of depression severity was tested. On the BDI-I, 41 patients scored in the normal range, 48 in the high normal range, and 57 in the depressed range previously linked to CHD prognosis. A BDI-I score in the depressed range was associated with a significantly greater likelihood of new/worsening impairment in myocardial perfusion from baseline to PS (odds ratio =2.89, 95% CI: 1.26 to 6.63, P=0.012). This remained significant in models controlling ACS recurrence/mortality risk factors and medications. There was no effect for selective serotonin reuptake inhibitor medications. Depressed patients with CHD are particularly susceptible to impairment in myocardial perfusion during PS. The confluence of PS with depression may contribute to a better understanding of the depression-associated risk for ACS recurrence and mortality. © 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

IL-6 signalling in patients with acute ST-elevation myocardial infarction

PubMed Central

Ritschel, Vibeke N.; Seljeflot, Ingebjørg; Arnesen, Harald; Halvorsen, Sigrun; Weiss, Thomas; Eritsland, Jan; Andersen, Geir Ø

2013-01-01

Cytokines of the IL-6 family have been related to infarct size and prognosis in patients with myocardial infarction. The aims of the present study were to elucidate possible associations between myocardial necrosis and left ventricular impairment and members of the IL-6 transsignalling system including soluble (s) IL-6R and (s) glycoprotein 130 (sgp130) in patients with ST-elevation myocardial infarction (STEMI) treated with primary PCI. In blood samples from 1028 STEMI patients, collected in-hosptial, we found significant correlations between peak TnT and IL-6 and CRP (p < 0.001, all) and between IL-6 and CRP and LV ejection fraction and NT-proBNP (p < 0.001, all). On the contrary, no significant associations were found between peak TnT and sgp130 or sIL-6R. Furthermore sgp130 was significantly elevated in diabetic patients and also associated with the glucometabolic state. In conclusion, circulating levels of IL-6 and CRP, but not the soluble forms of the receptor (sIL-6R) or the receptor signalling subunit (sgp130) were associated with the extent of myocardial necrosis. The biological importance of the IL-6/gp130-mediated signalling pathways in patients with acute myocardial infarction and dysglycemia should be further elucidated. PMID:24707455

Overexpression of Hsp20 Prevents Endotoxin-Induced Myocardial Dysfunction and Apoptosis via Inhibition of NF-κB Activation

PubMed Central

Wang, Xiaohong; Zingarelli, Basilia; Connor, Michael O’; Zhang, Pengyuan; Adeyemo, Adeola; Kranias, Evangelia G.; Wang, Yigang; Fan, Guo-Chang

2009-01-01

The occurrence of cardiovascular dysfunction in sepsis is associated with a significantly increased mortality rate of 70% to 90% compared with 20% in septic patients without cardiovascular impairment. Thus, rectification or blockade of myocardial depressant factors should partly ameliorate sepsis progression. Heat shock protein 20 (Hsp20) has been shown to enhance myocardial contractile function and protect against doxorubicin-induced cardiotoxicity. To investigate the possible role of Hsp20 in sepsis-mediated cardiac injury, we first examined the expression profiles of five major Hsps in response to lipopolysaccharide (LPS) challenge, and observed that only the expression of Hsp20 was downregulated in LPS-treated myocardium, suggesting that this decrease might be one of mechanisms contributing to LPS-induced cardiovascular defects. Further studies using loss-of-function and gain-of function approaches in adult rat cardiomyocytes verified that reduced Hsp20 levels were indeed correlated with the impaired contractile function. In fact, overexpression of Hsp20 significantly enhanced cardiomyocyte contractility upon LPS treatment. Moreover, after administration of LPS (25μg/g) in vivo, Hsp20 transgenic mice (10-fold overexpression) displayed: 1) an improvement in myocardial function; 2) reduced the degree of cardiac apoptosis; and 3) decreased NF-κB activity, accompanied with reduced myocardial cytokines IL-1β and TNF-α production, compared to the LPS-treated non-transgenic littermate controls. Thus, the increases in Hsp20 levels can protect against LPS-induced cardiac apoptosis and dysfunction, associated with inhibition of NF-κB activity, suggesting that Hsp20 may be a new therapeutic agent for the treatment of sepsis. PMID:19501592

[An analysis of the prognostic factors of acute myocardial infarction in different gender].

PubMed

Wang, Chun-Mei; Wu, Xue-Si; Han, Zhi-Hong; Zhang, Qian

2009-02-01

To analyse the prognostic factors of ST-elevation acute myocardial infarction men and women. The data of 904 in-hospital patients with ST-elevation myocardial infarction were collected from the database of our hospital during 2003 - 2004 and 728 of them were followed-up. The patients were divided into groups of male and female. Women had more accompanying diseases such as diabetes mellitus (DM) and hypertension than men; left ventricular ejection fraction (LVEF) was lower in female. The rate of successful reperfusion was lower in women than men (P < 0.05). Mortality rate was higher in women. 728 (202 female) patients were followed up. The use of beta-blockers were statistically different between two groups during follow-up. In the female group, LVEF was lower significantly and the rate of readmission for heart failure and myocardial infarction as well as that of mortality was higher (P < 0.05). Multivariate analysis showed that sex difference was an independent risk factor for in-hospital mortality (OR = 2.130, 95% CI 0.954 - 4.754, P = 0.045), but not for mortality in the followed-up period and readmission. There are many factors leading to the poor prognosis of ST-elevation acute myocardial infarction in women. It is essential to pay more attention to its clinical characteristics and begin intervention of the risk factors earlier so as to improve the prognosis.

Vitamin D Deficiency in Patients with Acute Myocardial Infarction: An Italian Single-Center Study.

PubMed

Aleksova, Aneta; Belfiore, Rita; Carriere, Cosimo; Kassem, Salam; La Carrubba, Salvatore; Barbati, Giulia; Sinagra, Gianfranco

2015-01-01

Hypovitaminosis D is a vitamin deficiency that has been increasing in developed countries; it was also suggested as an emerging risk factor for developing of atherosclerosis and acute myocardial infarction. The primary source of vitamin D is its cutaneous synthesis under exposure to sunlight. It has been suggested that 30 min of sun exposure twice weekly leads to sufficient vitamin D synthesis. The residents of Trieste (Italy) are well-known for their high exposure to sunlight in all seasons. We aimed to investigate the vitamin D status in subjects with acute myocardial infarction living in this area. Vitamin D status was identified in 478 subjects diagnosed with acute myocardial infarction. The median serum 25-hydroxyvitamin D concentration was 14.5 [7.8 - 22.7] ng/mL. Vitamin D deficiency and insufficiency were present in 324 (68 %) and 107 (22 %) subjects, respectively. Vitamin D deficiency was less frequent among subjects enrolled in the period from July to the end of September (p < 0.001). In a multivariate analysis vitamin D deficiency was predicted by older age (p = 0.02), female gender (p = 0.002), higher body mass index (p = 0.05), autumn/winter sampling (p < 0.001), increased parathyroid hormone (p = 0.03) and alkaline phosphatase (p = 0.003). We observed very high prevalence of vitamin D deficiency among subjects with myocardial infarction in all seasons of enrollment. However, it was lower in the summer when sun exposure is higher. The exposure to sunlight may be a cost-saving therapeutic strategy for the management of vitamin D deficiency.

Intratracheal Milrinone Bolus Administration During Acute Right Ventricular Dysfunction After Cardiopulmonary Bypass.

PubMed

Gebhard, Caroline Eva; Desjardins, Georges; Gebhard, Cathérine; Gavra, Paul; Denault, André Y

2017-04-01

To evaluate intratracheal milrinone (tMil) administration for rapid treatment of right ventricular (RV) dysfunction as a novel route after cardiopulmonary bypass. Retrospective analysis. Single-center study. The study comprised 7 patients undergoing cardiac surgery who exhibited acute RV dysfunction after cardiopulmonary bypass. After difficult weaning caused by cardiopulmonary bypass-induced acute RV dysfunction, milrinone was administered as a 5-mg bolus inside the endotracheal tube. RV function improvement, as indicated by decreasing pulmonary artery pressure and changes of RV waveforms, was observed in all 7 patients. Adverse effects of tMil included dynamic RV outflow tract obstruction (2 patients) and a decrease in systemic mean arterial pressure (1 patient). tMil may be an effective, rapid, and easily applicable therapeutic alternative to inhaled milrinone for the treatment of acute RV failure during cardiac surgery. However, sufficiently powered clinical trials are needed to confirm these findings. Copyright © 2017 Elsevier Inc. All rights reserved.

Postinfarct intramyocardial injection of mesenchymal stem cells pretreated with TGF-α improves acute myocardial function

PubMed Central

Herrmann, Jeremy L.; Abarbanell, Aaron M.; Weil, Brent R.; Wang, Yue; Poynter, Jeffrey A.; Manukyan, Mariuxi C.

2010-01-01

Stem cell-based therapies offer promising potential for myocardial infarction (MI), but endogenous molecules released in response to injury likely impair posttransplantation stem cell function. Stem cell-mediated cardioprotection occurs in part via paracrine effects, and transforming growth factor-α (TGF-α) has been shown to enhance paracrine function. However, it is unknown whether pretreating stem cells with TGF-α increases stem cell-mediated cardioprotection after acute MI. Mesenchymal stem cells (MSCs) were treated with TGF-α (250 ng/ml) for 24 h. Adult male Sprague-Dawley rat hearts were isolated and perfused using the Langendorff method. MI was induced by ligating the left anterior descending coronary artery. Postligation (30 min), vehicle or 1 × 106 MSCs with or without pretreatment were injected in the infarct border zones, and the hearts were perfused for an additional 60 min. Left ventricular function was continuously measured, and infarct size was assessed with Evans blue dye and 2,3,5-triphenyltetrazolium chloride staining. Myocardial production of interleukin (IL)-1β and IL-6 and caspase 3 activation was also measured. Left ventricular function decreased significantly following coronary artery ligation but improved following injection of untreated MSCs and to a greater extent after injection of pretreated MSCs. In addition, the infarct area, myocardial caspase 3 activation, and IL-6 production were lowest in hearts injected with pretreated cells. Intramyocardial injection of TGF-α-pretreated MSCs after acute MI is associated with increased myocardial function and decreased myocardial injury. This strategy may be useful for optimizing the therapeutic efficacy of stem cells for the treatment of acute MI. PMID:20484699

Static cardiomyoplasty with synthetic elastic net suppresses ventricular dilatation and dysfunction after myocardial infarction in the rat: a chronic study.

PubMed

Kato, Nobusuke; Kawaguchi, Akira T; Kishida, Akio; Yamaoka, Tetsuji

2013-07-01

Although static cardiomyoplasty prevents the left ventricle (LV) from dilatation, it may interfere with diastolic relaxation, or cause restriction. We developed a synthetic net with dual elasticity and tested its effect late after myocardial infarction in the rat. LV pressure-volume relationships (PVR) were successively analyzed before, after intravenous volume load, and 10 minutes after occlusion of the left anterior descending artery. Rats were then randomized into groups receiving synthetic net wrapping around the heart (NET+, n = 8) and only partially behind LV (NET-, n = 9), and they underwent the same PVR studies 6 weeks later. End-diastolic and end-systolic PVR were defined, and LV size and function were compared under standardized loading conditions. Although there was no difference in Day 0, increase in LV end-diastolic and end-systolic volumes were significantly attenuated in NET+ rats 6 weeks later when there was a significant correlation between LV volumes by PVR estimation and actual measurements, with significant differences in both measures between the groups: NET+ < NET-. The presence or absence of net did not show restrictive hemodynamics under acute volume load. Static cardiomyoplasty using a synthetic elastic net significantly attenuated LV dilatation and dysfunction without restriction late after myocardial infarction in the rat. © 2013, Copyright the Authors. Artificial Organs © 2013, International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.

Polycythemia vera presenting as acute myocardial infarction: An unusual presentation

PubMed Central

Bahbahani, Hussain; Aljenaee, Khaled; Bella, Abdelhaleem

2014-01-01

Acute myocardial infarction (AMI) is usually seen in the setting of atherosclerosis and its associated risk factors. Myocardial infarction in the young poses a particular challenge, as the disease is less likely, due to atherosclerosis. We report the case of a 37-year-old female patient who presented with ST segment elevation anterolateral AMI. The only abnormality on routine blood investigation was raised hemoglobin and hematocrit. After further testing, she was diagnosed according to the World Health Organization (WHO) criteria with polycythemia vera. This case illustrates the importance of recognizing polycythemia vera as an important cause of thrombosis, which can present initially as AMI, and to emphasize the early recognition of the disease in order to initiate appropriate management strategies. PMID:25544823

Psychological distress related to smoking cessation in patients with acute myocardial infarction

PubMed Central

Moreira-Santos, Thyego Mychell; Godoy, Irma; de Godoy, Ilda

2016-01-01

Among all causes of preventable deaths, smoking is responsible for the greatest number of deaths worldwide and predisposes to fatal, noncommunicable diseases, especially cardiovascular diseases. Lifestyle changes are effective in the treatment of patients with smoking-related diseases and assist in the prevention of premature mortality. Our objective was to investigate the available scientific evidence regarding the psychological distress related to smoking cessation in patients who have had acute myocardial infarction. To that end, we conducted an integrative review of the literature in order to summarize relevant studies on this topic. The selected databases were Scopus, PubMed Central, Institute for Scientific Information Web of Science (Core Collection), ScienceDirect, EMBASE, SciELO, LILACS e PsycINFO. On the basis of the inclusion and exclusion criteria adopted for this study, 14 articles were selected for analysis. Those studies showed that the prevalence of psychological distress is higher among smokers than among nonsmokers, and distress-related symptoms are much more common in smokers with acute myocardial infarction than in those without. Smoking cessation depends on the active participation of the smoker, whose major motivation is the underlying disease. Most studies have shown that there is a need to create treatment subgroups as a means of improving the treatment provided. This review article expands the knowledge regarding smoking cessation and shows the need to invest in future research that investigates subgroups of smokers diagnosed with the major smoking-related comorbidities, such as acute myocardial infarction, in order to develop specific interventions and psychological support strategies. PMID:26982043

Very late coronary spasm inducing acute myocardial infarction in a heart transplant recipient.

PubMed

Santoro, Francesco; Lopizzo, Agostino; Centola, Antonio; Cuculo, Andrea; Ruggiero, Antonio; Di Biase, Matteo; Brunetti, Natale Daniele

2016-12-01

: We report coronary angio findings of very late (10-year) coronary spasm inducing acute myocardial infarction with typical chest pain in a heart transplant recipient. Coronary spasm was promptly relieved by intra-coronary infusion of nitrates.

Comparison of hospital variation in acute myocardial infarction care and outcome between Sweden and United Kingdom: population based cohort study using nationwide clinical registries

PubMed Central

Sundström, Johan; Gale, Chris P; James, Stefan; Deanfield, John; Wallentin, Lars; Timmis, Adam; Jernberg, Tomas; Hemingway, Harry

2015-01-01

Objective To assess the between hospital variation in use of guideline recommended treatments and clinical outcomes for acute myocardial infarction in Sweden and the United Kingdom. Design Population based longitudinal cohort study using nationwide clinical registries. Setting and participants Nationwide registry data comprising all hospitals providing acute myocardial infarction care in Sweden (SWEDEHEART/RIKS-HIA, n=87; 119 786 patients) and the UK (NICOR/MINAP, n=242; 391 077 patients), 2004-10. Main outcome measures Between hospital variation in 30 day mortality of patients admitted with acute myocardial infarction. Results Case mix standardised 30 day mortality from acute myocardial infarction was lower in Swedish hospitals (8.4%) than in UK hospitals (9.7%), with less variation between hospitals (interquartile range 2.6% v 3.5%). In both countries, hospital level variation and 30 day mortality were inversely associated with provision of guideline recommended care. Compared with the highest quarter, hospitals in the lowest quarter for use of primary percutaneous coronary intervention had higher volume weighted 30 day mortality for ST elevation myocardial infarction (10.7% v 6.6% in Sweden; 12.7% v 5.8% in the UK). The adjusted odds ratio comparing the highest with the lowest quarters for hospitals’ use of primary percutaneous coronary intervention was 0.70 (95% confidence interval 0.62 to 0.79) in Sweden and 0.68 (0.60 to 0.76) in the UK. Differences in risk between hospital quarters of treatment for non-ST elevation myocardial infarction and secondary prevention drugs for all discharged acute myocardial infarction patients were smaller than for reperfusion treatment in both countries. Conclusion Between hospital variation in 30 day mortality for acute myocardial infarction was greater in the UK than in Sweden. This was associated with, and may be partly accounted for by, the higher practice variation in acute myocardial infarction guideline recommended

Comparison of hospital variation in acute myocardial infarction care and outcome between Sweden and United Kingdom: population based cohort study using nationwide clinical registries.

PubMed

Chung, Sheng-Chia; Sundström, Johan; Gale, Chris P; James, Stefan; Deanfield, John; Wallentin, Lars; Timmis, Adam; Jernberg, Tomas; Hemingway, Harry

2015-08-07

To assess the between hospital variation in use of guideline recommended treatments and clinical outcomes for acute myocardial infarction in Sweden and the United Kingdom. Population based longitudinal cohort study using nationwide clinical registries. Nationwide registry data comprising all hospitals providing acute myocardial infarction care in Sweden (SWEDEHEART/RIKS-HIA, n=87; 119,786 patients) and the UK (NICOR/MINAP, n=242; 391,077 patients), 2004-10. Between hospital variation in 30 day mortality of patients admitted with acute myocardial infarction. Case mix standardised 30 day mortality from acute myocardial infarction was lower in Swedish hospitals (8.4%) than in UK hospitals (9.7%), with less variation between hospitals (interquartile range 2.6% v 3.5%). In both countries, hospital level variation and 30 day mortality were inversely associated with provision of guideline recommended care. Compared with the highest quarter, hospitals in the lowest quarter for use of primary percutaneous coronary intervention had higher volume weighted 30 day mortality for ST elevation myocardial infarction (10.7% v 6.6% in Sweden; 12.7% v 5.8% in the UK). The adjusted odds ratio comparing the highest with the lowest quarters for hospitals' use of primary percutaneous coronary intervention was 0.70 (95% confidence interval 0.62 to 0.79) in Sweden and 0.68 (0.60 to 0.76) in the UK. Differences in risk between hospital quarters of treatment for non-ST elevation myocardial infarction and secondary prevention drugs for all discharged acute myocardial infarction patients were smaller than for reperfusion treatment in both countries. Between hospital variation in 30 day mortality for acute myocardial infarction was greater in the UK than in Sweden. This was associated with, and may be partly accounted for by, the higher practice variation in acute myocardial infarction guideline recommended treatment in the UK hospitals. High quality healthcare across all hospitals, especially

A pilot study of cardiac troponin I in patients with acute myocardial infarction and unstable angina.

PubMed

Selim, Najlaa A; Hmouda, Houssem T

2002-05-01

To assess the value of cardiac troponin I in the initial management of acute myocardial infarction and unstable angina, as well as the concordance between creatine phosphokinase-cardiac isoenzyme and cardiac troponin I. We reviewed retrospectively the charts of 32 patients with acute myocardial infarction or unstable angina admitted to the Intensive Care Unit from the Emergency Room of King Khalid Military City Hospital, Hafar-Al-Batin, Kingdom of Saudi Arabia from April 1998 to September 2000. The time of admission to the intensive care unit, which corresponds to the beginning of thrombolytic therapy, the time when cardiac enzymes (creatine phosphokinase-cardiac isoenzyme and cardiac troponin I) are available as well as number of cardiac troponin I determinations before obtaining a significant positive result (>2ng/ml) and the delay between admission and the first significant positive result of cardiac troponin I, were evaluated. Sixteen patients had confirmed acute myocardial infarction based on the association of typical chest pain, electrocardiographic findings with ST segment elevation and significant increase of the ratio creatine phosphokinase-cardiac isoenzyme/creatine phosphokinase > 10%. Sixteen patients had unstable angina and out of the 16 patients (81.25%) with acute myocardial infarction, 13 received thrombolytic therapy which was initiated on the basis of typical clinical history and electrocardiographic features, before the availability of cardiac enzymes. Troponin I was available in only 13 cases. The number of tests performed in these patients was 32. The first positive result of cardiac troponin I was available within a mean time of 16.66 20.8 hours from admission. The number of negative tests performed before obtaining a frank positive result was 9 in 12 patients. The number of positive tests after having obtained the first frank positive cardiac troponin I result was 10 in 12 patients. In all cases of cardiac troponin I, results were concordant

Acute myocardial infarction associated with blood transfusion: case report and literature review.

PubMed

Velibey, Yalcin; Erbay, Aliriza; Ozkurt, Enver; Usta, Emrah; Akin, Filiz

2014-04-01

A 62-year old patient with a history of chronic anemia associated with malabsorption secondary to short gut syndrome, experienced acute chest pain the second hour after the transfusion of a crossmatch-compatible erythrocyte suspension. His electrocardiogram (ECG) revealed widespread ST-segment depressions and he had an elevated troponin level. Laboratory findings and physical examination did not indicate the presence of immunological or non-immunological blood transfusion reactions. Cardiac catheterization was performed and showed angiographically non-obstructive, atherosclerotic plaques and the absence of vasospasm or thrombus formation. Following antiischemic therapy his symptoms resolved completely. The ECG obtained 24 hours after the emergence of chest pain demonstrated normal sinus rhythm with no ST-T wave changes. We present a rare case of acute myocardial infarction induced following a blood transfusion. To the best of our knowledge, a few cases of acute myocardial infarction associated with blood transfusion have been formally recorded in the medical literature and the clinical experience regarding such cases is indeed quite limited. The present case is reviewed in the context of the relevant literature as a practical resource for clinical practice. Crown Copyright © 2014. Published by Elsevier Ltd. All rights reserved.

Right Ventricular Dysfunction in Chronic Lung Disease

PubMed Central

Kolb, Todd M.; Hassoun, Paul M.

2012-01-01

Right ventricular dysfunction arises in chronic lung disease when chronic hypoxemia and disruption of pulmonary vascular beds contribute to increase ventricular afterload, and is generally defined by hypertrophy with preserved myocardial contractility and cardiac output. Although the exact prevalence is unknown, right ventricular hypertrophy appears to be a common complication of chronic lung disease, and more frequently complicates advanced lung disease. Right ventricular failure is rare, except during acute exacerbations of chronic lung disease or when multiple co-morbidities are present. Treatment is targeted at correcting hypoxia and improving pulmonary gas exchange and mechanics. There are presently no convincing data to support the use of pulmonary hypertension-specific therapies in patients with right ventricular dysfunction secondary to chronic lung disease. PMID:22548815

Acute Myocardial Infarction: Changes in Patient Characteristics, Management, and 6-Month Outcomes Over a Period of 20 Years in the FAST-MI Program (French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction) 1995 to 2015.

PubMed

Puymirat, Etienne; Simon, Tabassome; Cayla, Guillaume; Cottin, Yves; Elbaz, Meyer; Coste, Pierre; Lemesle, Gilles; Motreff, Pascal; Popovic, Batric; Khalife, Khalife; Labèque, Jean-Noel; Perret, Thibaut; Le Ray, Christophe; Orion, Laurent; Jouve, Bernard; Blanchard, Didier; Peycher, Patrick; Silvain, Johanne; Steg, Philippe Gabriel; Goldstein, Patrick; Guéret, Pascal; Belle, Loic; Aissaoui, Nadia; Ferrières, Jean; Schiele, François; Danchin, Nicolas

2017-11-14

ST-segment-elevation myocardial infarction (STEMI) and non-ST-segment-elevation myocardial infarction (NSTEMI) management has evolved considerably over the past 2 decades. Little information on mortality trends in the most recent years is available. We assessed trends in characteristics, treatments, and outcomes for acute myocardial infarction in France between 1995 and 2015. We used data from 5 one-month registries, conducted 5 years apart, from 1995 to 2015, including 14 423 patients with acute myocardial infarction (59% STEMI) admitted to cardiac intensive care units in metropolitan France. From 1995 to 2015, mean age decreased from 66±14 to 63±14 years in patients with STEMI; it remained stable (68±14 years) in patients with NSTEMI, whereas diabetes mellitus, obesity, and hypertension increased. At the acute stage, intended primary percutaneous coronary intervention increased from 12% (1995) to 76% (2015) in patients with STEMI. In patients with NSTEMI, percutaneous coronary intervention ≤72 hours from admission increased from 9% (1995) to 60% (2015). Six-month mortality consistently decreased in patients with STEMI from 17.2% in 1995 to 6.9% in 2010 and 5.3% in 2015; it decreased from 17.2% to 6.9% in 2010 and 6.3% in 2015 in patients with NSTEMI. Mortality still decreased after 2010 in patients with STEMI without reperfusion therapy, whereas no further mortality gain was found in patients with STEMI with reperfusion therapy or in patients with NSTEMI, whether or not they were treated with percutaneous coronary intervention. Over the past 20 years, 6-month mortality after acute myocardial infarction has decreased considerably for patients with STEMI and NSTEMI. Mortality figures continued to decline in patients with STEMI until 2015, whereas mortality in patients with NSTEMI appears stable since 2010. © 2017 American Heart Association, Inc.

Alteration of Multiple Leukocyte Gene Expression Networks is Linked with Magnetic Resonance Markers of Prognosis After Acute ST-Elevation Myocardial Infarction.

PubMed

Teren, A; Kirsten, H; Beutner, F; Scholz, M; Holdt, L M; Teupser, D; Gutberlet, M; Thiery, J; Schuler, G; Eitel, I

2017-02-03

Prognostic relevant pathways of leukocyte involvement in human myocardial ischemic-reperfusion injury are largely unknown. We enrolled 136 patients with ST-elevation myocardial infarction (STEMI) after primary angioplasty within 12 h after onset of symptoms. Following reperfusion, whole blood was collected within a median time interval of 20 h (interquartile range: 15-25 h) for genome-wide gene expression analysis. Subsequent CMR scans were performed using a standard protocol to determine infarct size (IS), area at risk (AAR), myocardial salvage index (MSI) and the extent of late microvascular obstruction (lateMO). We found 398 genes associated with lateMO and two genes with IS. Neither AAR, nor MSI showed significant correlations with gene expression. Genes correlating with lateMO were strongly related to several canonical pathways, including positive regulation of T-cell activation (p = 3.44 × 10 -5 ), and regulation of inflammatory response (p = 1.86 × 10 -3 ). Network analysis of multiple gene expression alterations associated with larger lateMO identified the following functional consequences: facilitated utilisation and decreased concentration of free fatty acid, repressed cell differentiation, enhanced phagocyte movement, increased cell death, vascular disease and compensatory vasculogenesis. In conclusion, the extent of lateMO after acute, reperfused STEMI correlated with altered activation of multiple genes related to fatty acid utilisation, lymphocyte differentiation, phagocyte mobilisation, cell survival, and vascular dysfunction.

Income inequality and 30 day outcomes after acute myocardial infarction, heart failure, and pneumonia: retrospective cohort study.

PubMed

Lindenauer, Peter K; Lagu, Tara; Rothberg, Michael B; Avrunin, Jill; Pekow, Penelope S; Wang, Yongfei; Krumholz, Harlan M

2013-02-14

To examine the association between income inequality and the risk of mortality and readmission within 30 days of hospitalization. Retrospective cohort study of Medicare beneficiaries in the United States. Hierarchical, logistic regression models were developed to estimate the association between income inequality (measured at the US state level) and a patient's risk of mortality and readmission, while sequentially controlling for patient, hospital, other state, and patient socioeconomic characteristics. We considered a 0.05 unit increase in the Gini coefficient as a measure of income inequality. US acute care hospitals. Patients aged 65 years and older, and hospitalized in 2006-08 with a principal diagnosis of acute myocardial infarction, heart failure, or pneumonia. Risk of death within 30 days of admission or rehospitalization for any cause within 30 days of discharge. The potential number of excess deaths and readmissions associated with higher levels of inequality in US states in the three highest quarters of income inequality were compared with corresponding data in US states in the lowest quarter. Mortality analyses included 555,962 admissions (4348 hospitals) for acute myocardial infarction, 1,092,285 (4484) for heart failure, and 1,146,414 (4520); readmission analyses included 553,037 (4262), 1,345,909 (4494), and 1,345,909 (4524) admissions, respectively. In 2006-08, income inequality in US states (as measured by the average Gini coefficient over three years) varied from 0.41 in Utah to 0.50 in New York. Multilevel models showed no significant association between income inequality and mortality within 30 days of admission for patients with acute myocardial infarction, heart failure, or pneumonia. By contrast, income inequality was associated with rehospitalization (acute myocardial infarction, risk ratio 1.09 (95% confidence interval 1.03 to 1.15), heart failure 1.07 (1.01 to 1.12), pneumonia 1.09 (1.03 to 1.15)). Further adjustment for individual income

Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlled trial: the Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial.

PubMed

Mahaffey, K W; Puma, J A; Barbagelata, N A; DiCarli, M F; Leesar, M A; Browne, K F; Eisenberg, P R; Bolli, R; Casas, A C; Molina-Viamonte, V; Orlandi, C; Blevins, R; Gibbons, R J; Califf, R M; Granger, C B

1999-11-15

The Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial was designed to test the hypothesis that adenosine as an adjunct to thrombolysis would reduce myocardial infarct size. Reperfusion therapy for acute myocardial infarction (MI) has been shown to reduce mortality, but reperfusion itself also may have deleterious effects. The AMISTAD trial was a prospective, open-label trial of thrombolysis with randomization to adenosine or placebo in 236 patients within 6 h of infarction onset. The primary end point was infarct size as determined by Tc-99 m sestamibi single-photon emission computed tomography (SPECT) imaging 6+/-1 days after enrollment based on multivariable regression modeling to adjust for covariates. Secondary end points were myocardial salvage index and a composite of in-hospital clinical outcomes (death, reinfarction, shock, congestive heart failure or stroke). In all, 236 patients were enrolled. Final infarct size was assessed in 197 (83%) patients. There was a 33% relative reduction in infarct size (p = 0.03) with adenosine. There was a 67% relative reduction in infarct size in patients with anterior infarction (15% in the adenosine group vs. 45.5% in the placebo group) but no reduction in patients with infarcts located elsewhere (11.5% for both groups). Patients randomized to adenosine tended to reach the composite clinical end point more often than those assigned to placebo (22% vs. 16%; odds ratio, 1.43; 95% confidence interval, 0.71 to 2.89). Many agents thought to attenuate reperfusion injury have been unsuccessful in clinical investigation. In this study, adenosine resulted in a significant reduction in infarct size. These data support the need for a large clinical outcome trial.

[Takotsubo cardiomiopathy. A rare cause of cardiogenic shock simulating acute myocardial infarction].

PubMed

Vasconcelos, Jayro Thadeu Paiva de; Martins, Sebastião; Sousa, João Francisco de; Portela, Antenor

2005-08-01

Takotsubo Cardiomiopathy is a rare cause of acute left ventricular aneurysm, in the absence of coronariopathy, only recently described in world literature. Symptoms may be similar to those from acute myocardial infarction with typical thoracic pain. The image of dumbbell or Takotsubo (a device used in Japan to capture octopus) suggestive ventricular ballooning is characteristic of that new syndrome and there is usually the disappearing of dyskinetic movement up to the 18th day from the beginning of the symptoms, in average.

Investigation of the effects of intravenous magnesium sulphate on cardiac rhythm in acute myocardial infarction.

PubMed Central

Roffe, C.; Fletcher, S.; Woods, K. L.

1994-01-01

OBJECTIVE--To examine the effect of doubling serum magnesium concentration on the incidence of arrhythmias in patients with suspected acute myocardial infarction. DESIGN--Randomised double blind clinical trial. SETTING--Coronary care unit of a teaching hospital. PATIENTS--Clinical data were collected on 2316 randomised patients with suspected acute myocardial infarction. Holter monitoring was performed in a subgroup of 70 patients and analysed in 48 patients in whom acute myocardial infarction was confirmed. INTERVENTIONS--By random allocation, patients received either an intravenous loading dose of 8 mmol magnesium sulphate over five minutes plus 65 mmol over the next 24 hours, or equal volumes of saline. MAIN OUTCOME MEASURES--(a) Clinically documented arrhythmias; (b) use of antiarrhythmic treatments, cardioversion, and insertion of a pacemaker; (c) incidence of all abnormal rhythms during Holter monitoring. RESULTS--In the main trial the incidence of rhythm disturbance while in the coronary care unit (expressed as the odds ratio (OR) for magnesium: placebo and its 95% confidence interval) was not significantly different between treatment groups for ventricular fibrillation (OR 0.74; 0.46 to 1.20), ventricular tachycardia (OR 0.87; 0.63 to 1.20), supraventricular tachycardia (OR 0.69; 0.38 to 1.26), atrial fibrillation (OR 0.92; 0.69 to 1.23), or heart block of any degree (OR 1.17; 0.83 to 1.65). Sinus bradycardia was significantly more common in the magnesium group (OR 1.38; 1.03 to 1.85; p = 0.02). These findings were corroborated by the use of treatments for rhythm disturbance and the data from Holter monitoring. CONCLUSION--The regimen of intravenous magnesium sulphate used here had no significant effect on arrhythmia in acute myocardial infarction. The reduction in mortality that has been shown with this form of treatment is not attributable to suppression of life threatening rhythm disturbances. PMID:8130021

Lin28a protects against postinfarction myocardial remodeling and dysfunction through Sirt1 activation and autophagy enhancement.

PubMed

Hao, Yuanyuan; Lu, Qun; Yang, Guodong; Ma, Aiqun

2016-10-28

Myocardial remodeling and cardiac dysfunction prevention may represent a therapeutic approach to reduce mortality in patients with myocardial infarction (MI). We investigated the effects of Lin28a in experimental MI models, as well as the mechanisms underlying these effects. Left anterior descending (LAD) coronary artery ligation was used to construct an MI-induced injury model. Neonatal cardiomyocytes were isolated and cultured to investigate the mechanisms underlying the protective effects of Lin28a against MI-induced injury. Lin28a significantly inhibited left ventricular remodeling and cardiac dysfunction after MI, as demonstrated via echocardiography and hemodynamic measurements. Lin28a reduced cardiac enzyme and inflammatory marker release in mice subjected to MI-induced injury. The mechanisms underlying the protective effects of Lin28a against MI-induced injury were associated with autophagy enhancements and apoptosis inhibition. Consistent with these findings, Lin28a knockdown aggravated cardiac remodeling and dysfunction after MI-induced injury. Lin28a knockdown also inhibited cardiomyocyte autophagy and increased cardiomyocyte apoptosis in mice subjected to MI-induced injury. Interestingly, Sirt1 knockdown abolished the protective effects of Lin28a against cardiac remodeling and dysfunction after MI, and Lin28a failed to increase the numbers of GFP-LC3-positive punctae and decrease aggresome and p62 accumulation in Sirt1-knockdown neonatal cardiomyocytes subjected to hypoxia-induced injury. Lin28a inhibits cardiac remodeling, improves cardiac function, and reduces cardiac enzyme and inflammatory marker release after MI. Lin28a also up-regulates cardiomyocyte autophagy and inhibits cardiomyocyte apoptosis through Sirt1 activation. Copyright © 2016 Elsevier Inc. All rights reserved.

Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction.

PubMed

Bobi, Joaquim; Solanes, Núria; Fernández-Jiménez, Rodrigo; Galán-Arriola, Carlos; Dantas, Ana Paula; Fernández-Friera, Leticia; Gálvez-Montón, Carolina; Rigol-Monzó, Elisabet; Agüero, Jaume; Ramírez, José; Roqué, Mercè; Bayés-Genís, Antoni; Sánchez-González, Javier; García-Álvarez, Ana; Sabaté, Manel; Roura, Santiago; Ibáñez, Borja; Rigol, Montserrat

2017-05-03

Autologous adipose tissue-derived mesenchymal stem cells (ATMSCs) therapy is a promising strategy to improve post-myocardial infarction outcomes. In a porcine model of acute myocardial infarction, we studied the long-term effects and the mechanisms involved in allogeneic ATMSCs administration on myocardial performance. Thirty-eight pigs underwent 50 minutes of coronary occlusion; the study was completed in 33 pigs. After reperfusion, allogeneic ATMSCs or culture medium (vehicle) were intracoronarily administered. Follow-ups were performed at short (2 days after acute myocardial infarction vehicle-treated, n=10; ATMSCs-treated, n=9) or long term (60 days after acute myocardial infarction vehicle-treated, n=7; ATMSCs-treated, n=7). At short term, infarcted myocardium analysis showed reduced apoptosis in the ATMSCs-treated animals (48.6±6% versus 55.9±5.7% in vehicle; P =0.017); enhancement of the reparative process with up-regulated vascular endothelial growth factor, granulocyte macrophage colony-stimulating factor, and stromal-derived factor-1α gene expression; and increased M2 macrophages (67.2±10% versus 54.7±10.2% in vehicle; P =0.016). In long-term groups, increase in myocardial perfusion at the anterior infarct border was observed both on day-7 and day-60 cardiac magnetic resonance studies in ATMSCs-treated animals, compared to vehicle (87.9±28.7 versus 57.4±17.7 mL/min per gram at 7 days; P =0.034 and 99±22.6 versus 43.3±14.7 22.6 mL/min per gram at 60 days; P =0.0001, respectively). At day 60, higher vascular density was detected at the border zone in the ATMSCs-treated animals (118±18 versus 92.4±24.3 vessels/mm 2 in vehicle; P =0.045). Cardiac magnetic resonance-measured left ventricular ejection fraction of left ventricular volumes was not different between groups at any time point. In this porcine acute myocardial infarction model, allogeneic ATMSCs-based therapy was associated with increased cardioprotective and reparative

The effect of optimal medical therapy on 1-year mortality after acute myocardial infarction.

PubMed

Bramlage, P; Messer, C; Bitterlich, N; Pohlmann, C; Cuneo, A; Stammwitz, E; Tebbenjohanns, J; Gohlke, H; Senges, J; Tebbe, U

2010-04-01

Five drug classes have been shown to improve the prognosis of acute myocardial infarction in clinical trials: aspirin, beta-blockers, statins, renin angiotensin system (RAS) blockers and thienopyridines. We aimed to assess whether the benefits of combining these drugs (termed optimal medical therapy, OMT), will result in a reduction of mortality in clinical practice. Nationwide registry Hospitals with a cardiology unit or internal medicine department. 5353 patients with acute myocardial infarction. At hospital discharge 89% received aspirin, 90% beta-blockers, 84% statins, 81% RAS blockers, 70% a thienopyridine and 46.2% OMT. Pharmacotherapy OR with 95% CI for mortality from myocardial infarction were calculated and adjusted for patient risk at baseline. Total mortality was reduced by 74% in patients receiving OMT (adj OR 0.26; 95% CI 0.18 to 0.38) versus patients receiving one or no drug. This was consistent in subgroups defined by STEMI/NSTEMI, diabetes and gender. Mortality was also reduced in patients receiving 2-4 drugs (adj OR 0.49; 95% CI 0.35 to 0.68), diabetic patients being the only subgroup with no significant effect. Analyses on the relative importance of either component revealed that withdrawal of beta-blockers (adj OR 0.63; 95% CI 0.34 to 1.16) and/or a combination of aspirin/clopidogrel (adj OR 0.59; 95% CI 0.20 to 1.17) abolished the risk reduction conferred by OMT. OMT over 1 year was associated with a significantly lower mortality of patients with acute myocardial infarction in clinical practice. However OMT is provided to less than half of eligible patients leaving room for substantial improvement.

Inflammatory response, neutrophil activation, and free radical production after acute myocardial infarction: effect of thrombolytic treatment.

PubMed Central

Bell, D; Jackson, M; Nicoll, J J; Millar, A; Dawes, J; Muir, A L

1990-01-01

Activated neutrophils releasing proteolytic enzymes and oxygen free radicals have been implicated in extending myocardial injury after myocardial infarction. Neutrophil elastase was used as a marker of neutrophil activation and the non-peroxide diene conjugate of linoleic acid was used as an indicator of free radical activity in 32 patients after acute myocardial infarction; 17 were treated by intravenous thrombolysis. Patients with acute myocardial infarction had higher plasma concentrations of neutrophil elastase and the non-peroxide diene conjugated isomer of linoleic acid than normal volunteers or patients with stable ischaemic heart disease. Patients treated by thrombolysis had an early peak of neutrophil elastase at eight hours while those who had not been treated by thrombolysis showed a later peak 40 hours after infarction. The plasma concentration of non-peroxide conjugated diene of linoleic acid was highest 16 hours after the infarction irrespective of treatment by thrombolysis. Quantitative imaging with single photon emission tomography showed decreased uptake of indium-111 labelled neutrophils in the infarcted myocardium (as judged from technetium-99m pyrophosphate) in those who had received thrombolysis, suggesting a decreased inflammatory response. The results indicate increased neutrophil activation and free radical production after myocardial infarction; they also suggest that thrombolysis does not amplify the inflammatory response and may indeed suppress it. Images PMID:2317413

Dunye Guanxinning Improves Acute Myocardial Ischemia-Reperfusion Injury by Inhibiting Neutrophil Infiltration and Caspase-1 Activity

PubMed Central

Zhang, Q. G.; Wang, S. R.; Chen, X. M.; Guo, H. N.

2018-01-01

Acute myocardial infarction is the most serious manifestation of cardiovascular disease, and it is a life-threatening condition. Dunye Guanxinning (DG) is a protective traditional Chinese patent herbal medicine with high clinical efficacy and suitable for the treatment of myocardial infarction. However, the mechanism through which it is beneficial is unclear. In this study, we hypothesized that DG improves acute myocardial ischemia-reperfusion injury by inhibiting neutrophil infiltration and caspase-1 activity. We found that DG administration decreased infarct size and cardiomyocyte apoptosis and improved left ventricular ejection fraction, fractional shortening, end-systolic volume index, end-systolic diameter, and carotid arterial blood flow output in rats. DG administration also improved hemorheological parameters, myocardial damage biomarkers, and oxidative stress indexes. The findings showed that DG administration inhibited neutrophil infiltration and reduced the serum interleukin-1 beta (IL-1β) level and myocardial IL-1β maturation. Moreover, DG administration inhibited caspase-1 activity and activated adenosine monophosphate-activated protein kinase (AMPK) phosphorylation in rat hearts. These results suggested that DG administration inhibits inflammasome activity and IL-1β release through the AMPK pathway. Our findings support the clinical efficacy of DG and partially reveal its mechanism, which is beneficial for understanding the therapeutic effects of this protective traditional Chinese patent drug. PMID:29674944

Is delayed surgical revascularization in acute myocardial infarction useful or dangerous? New insights into an old problem.

PubMed

Grieshaber, Philippe; Roth, Peter; Oster, Lukas; Schneider, Tobias M; Görlach, Gerold; Nieman, Bernd; Böning, Andreas

2017-11-01

Haemodynamically stable patients admitted for coronary artery bypass grafting in acute myocardial infarction often undergo delayed surgery in order to avoid the risks of emergency surgery. However, initially stable patients undergoing delayed surgery may develop low cardiac output syndrome (LCOS) during the waiting period, which might be a major drawback of this strategy. We aim to define risk factors and clinical consequences of LCOS during the waiting period. A total of 530 consecutive patients with acute myocardial infarction (33% non-ST-segment elevation myocardial infarction and 67% ST-segment-elevation myocardial infarction) underwent isolated coronary artery bypass grafting between 2008 and 2013. Outcomes after either immediate (<48 h after onset of symptoms) or delayed (>48 h after onset of symptoms) therapy were compared. Predictors of preoperative development of LCOS were identified using multivariate regression analysis. Of the 327 patients undergoing delayed therapy, 39 (12%) developed preoperative LCOS, resulting in increased mortality compared with patients who remained stable (21 vs 7.6%, P < 0.001). Immediate therapy resulted in similar mortality compared with delayed therapy (6.4 vs 7.6%; P = 0.68) and better 7-year survival (70 vs 55%; P < 0.001). Predictors of developing LCOS were reduced left ventricular function (odds ratio 4.4), renal impairment (odds ratio 3.0), acute pulmonary infection (odds ratio 3.4) and the extent of troponin elevation at admission (odds ratio 1.01 per increase by 1 µg/l). In patients with acute myocardial infarction undergoing delayed coronary artery bypass grafting, preoperative LCOS is a relevant and dangerous condition that can be avoided by operating immediately or by carefully selecting patients to be delayed according to the risk parameters identified preoperatively. © The Author 2017. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All

Folic acid prevents cardiac dysfunction and reduces myocardial fibrosis in a mouse model of high-fat diet-induced obesity.

PubMed

Li, Wei; Tang, Renqiao; Ouyang, Shengrong; Ma, Feifei; Liu, Zhuo; Wu, Jianxin

2017-01-01

Folic acid (FA) is an antioxidant that can reduce reactive oxygen species generation and can blunt cardiac dysfunction during ischemia. We hypothesized that FA supplementation prevents cardiac fibrosis and cardiac dysfunction induced by obesity. Six-week-old C57BL6/J mice were fed a high-fat diet (HFD), normal diet (ND), or an HFD supplemented with folic acid (FAD) for 14 weeks. Cardiac function was measured using a transthoracic echocardiographic exam. Phenotypic analysis included measurements of body and heart weight, blood glucose and tissue homocysteine (Hcy) content, and heart oxidative stress status. HFD consumption elevated fasting blood glucose levels and caused obesity and heart enlargement. FA supplementation in HFD-fed mice resulted in reduced fasting blood glucose, heart weight, and heart tissue Hcy content. We also observed a significant cardiac systolic dysfunction when mice were subjected to HFD feeding as indicated by a reduction in the left ventricular ejection fraction and fractional shortening. However, FAD treatment improved cardiac function. FA supplementation protected against cardiac fibrosis induced by HFD. In addition, HFD increased malondialdehyde concentration of the heart tissue and reduced the levels of antioxidant enzyme, glutathione, and catalase. HFD consumption induced myocardial oxidant stress with amelioration by FA treatment. FA supplementation significantly lowers blood glucose levels and heart tissue Hcy content and reverses cardiac dysfunction induced by HFD in mice. These functional improvements of the heart may be mediated by the alleviation of oxidative stress and myocardial fibrosis.

Attenuating the defibrillation dosage decreases postresuscitation myocardial dysfunction in a swine model of pediatric ventricular fibrillation

PubMed Central

Berg, Marc D.; Banville, Isabelle L.; Chapman, Fred W.; Walker, Robert G.; Gaballa, Mohammed A.; Hilwig, Ronald W.; Samson, Ricardo A.; Kern, Karl B.; Berg, Robert A.

2009-01-01

Objective The optimal biphasic defibrillation dose for children is unknown. Postresuscitation myocardial dysfunction is common and may be worsened by higher defibrillation doses. Adult-dose automated external defibrillators are commonly available; pediatric doses can be delivered by attenuating the adult defibrillation dose through a pediatric pads/cable system. The objective was to investigate whether unattenuated (adult) dose biphasic defibrillation results in greater postresuscitation myocardial dysfunction and damage than attenuated (pediatric) defibrillation. Design Laboratory animal experiment. Setting University animal laboratory. Subjects Domestic swine weighing 19 ± 3.6 kg. Interventions Fifty-two piglets were randomized to receive biphasic defibrillation using either adult-dose shocks of 200, 300, and 360 J or pediatric-dose shocks of ~50, 75, and 85 J after 7 mins of untreated ventricular fibrillation. Contrast left ventriculograms were obtained at baseline and then at 1, 2, 3, and 4 hrs postresuscitation. Postresuscitation left ventricular ejection fraction and cardiac troponins were evaluated. Measurements and Main Results By design, piglets in the adult-dose group received shocks with more energy (261 ± 65 J vs. 72 ± 12 J, p < .001) and higher peak current (37 ± 8 A vs. 13 ± 2 A, p < .001) at the largest defibrillation dose needed. In both groups, left ventricular ejection fraction was reduced significantly at 1, 2, and 4 hrs from baseline and improved during the 4 hrs postresuscitation. The decrease in left ventricular ejection fraction from baseline was greater after adult-dose defibrillation. Plasma cardiac troponin levels were elevated 4 hrs postresuscitation in 11 of 19 adult-dose piglets vs. four of 20 pediatric-dose piglets (p = .02). Conclusions Unattenuated adult-dose defibrillation results in a greater frequency of myocardial damage and worse postresuscitation myocardial function than pediatric doses in a swine model of prolonged out

Neural mechanisms and delayed gastric emptying of liquid induced through acute myocardial infarction in rats.

PubMed

Nunez, Wilson Ranu Ramirez; Ozaki, Michiko Regina; Vinagre, Adriana Mendes; Collares, Edgard Ferro; Almeida, Eros Antonio de

2015-02-01

In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE) of liquid in rats. Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABAB receptors and also participation of paraventricular nucleus (PVN) of the hypothalamus in GE and gastric compliance (GC) in infarcted rats. Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH) group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABAB receptors, baclofen was injected via icv (intracerebroventricular). Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1 mA/10 s electrical current and GE was determined by measuring the percentage of gastric retention (% GR) of a saline meal. No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABAB receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN.

Myocardial Rupture in Acute Myocardial Infarction: Mechanistic Explanation Based on the Ventricular Myocardial Band Hypothesis.

PubMed

Vargas-Barron, Jesús; Antunez-Montes, Omar-Yassef; Roldán, Francisco-Javier; Aranda-Frausto, Alberto; González-Pacheco, Hector; Romero-Cardenas, Ángel; Zabalgoitia, Miguel

2015-01-01

Torrent-Guasp explains the structure of the ventricular myocardium by means of a helical muscular band. Our primary purpose was to demonstrate the utility of echocardiography in human and porcine hearts in identifying the segments of the myocardial band. The second purpose was to evaluate the relation of the topographic distribution of the myocardial band with some post-myocardial infarction ruptures. Five porcine and one human heart without cardiopathy were dissected and the ventricular myocardial segments were color-coded for illustration and reconstruction purposes. These segments were then correlated to the conventional echocardiographic images. Afterwards in three cases with post-myocardial infarction rupture, a correlation of the topographic location of the rupture with the distribution of the ventricular band was made. The human ventricular band does not show any differences from the porcine band, which confirms the similarities of the four segments; these segments could be identified by echocardiography. In three cases with myocardial rupture, a correlation of the intra-myocardial dissection with the distribution of the ventricular band was observed. Echocardiography is helpful in identifying the myocardial band segments as well as the correlation with the topographic distribution of some myocardial post-infarction ruptures.

Stress Induced Cardiomyopathy Triggered by Acute Myocardial Infarction: A Case Series Challenging the Mayo Clinic Definition.

PubMed

Christodoulidis, Georgios; Kundoor, Vishwa; Kaluski, Edo

2017-08-28

BACKGROUND Various physical and emotional factors have been previously described as triggers for stress induced cardiomyopathy. However, acute myocardial infarction as a trigger has never been reported. CASE REPORT We describe four patients who presented with an acute myocardial infarction, in whom the initial echocardiography revealed wall motion abnormalities extending beyond the coronary distribution of the infarct artery. Of the four patients identified, the mean age was 59 years; three patients were women and two patients had underlying psychiatric history. Electrocardiogram revealed ST elevation in the anterior leads in three patients; QTc was prolonged in all cases. All patients had ≤ moderately elevated troponin. Single culprit lesion was found uniformly in the proximal or mid left anterior descending artery. Initial echocardiography revealed severely reduced ejection fraction with relative sparing of the basal segments, whereas early repeat echocardiography revealed significant improvement in the left ventricular function in all patients. CONCLUSIONS This is the first case series demonstrating that acute myocardial infarction can trigger stress induced cardiomyopathy. Extensive reversible wall motion abnormalities, beyond the ones expected from angiography, accompanied by modest elevation in troponin and marked QTc prolongation, suggest superimposed stress induced cardiomyopathy.

Cardiac macrophages promote diastolic dysfunction.

PubMed

Hulsmans, Maarten; Sager, Hendrik B; Roh, Jason D; Valero-Muñoz, María; Houstis, Nicholas E; Iwamoto, Yoshiko; Sun, Yuan; Wilson, Richard M; Wojtkiewicz, Gregory; Tricot, Benoit; Osborne, Michael T; Hung, Judy; Vinegoni, Claudio; Naxerova, Kamila; Sosnovik, David E; Zile, Michael R; Bradshaw, Amy D; Liao, Ronglih; Tawakol, Ahmed; Weissleder, Ralph; Rosenzweig, Anthony; Swirski, Filip K; Sam, Flora; Nahrendorf, Matthias

2018-02-05

Macrophages populate the healthy myocardium and, depending on their phenotype, may contribute to tissue homeostasis or disease. Their origin and role in diastolic dysfunction, a hallmark of cardiac aging and heart failure with preserved ejection fraction, remain unclear. Here we show that cardiac macrophages expand in humans and mice with diastolic dysfunction, which in mice was induced by either hypertension or advanced age. A higher murine myocardial macrophage density results from monocyte recruitment and increased hematopoiesis in bone marrow and spleen. In humans, we observed a parallel constellation of hematopoietic activation: circulating myeloid cells are more frequent, and splenic 18 F-FDG PET/CT imaging signal correlates with echocardiographic indices of diastolic dysfunction. While diastolic dysfunction develops, cardiac macrophages produce IL-10, activate fibroblasts, and stimulate collagen deposition, leading to impaired myocardial relaxation and increased myocardial stiffness. Deletion of IL-10 in macrophages improves diastolic function. These data imply expansion and phenotypic changes of cardiac macrophages as therapeutic targets for cardiac fibrosis leading to diastolic dysfunction. © 2018 Hulsmans et al.

Right Ventricular Myocardial Stiffness in Experimental Pulmonary Arterial Hypertension

PubMed Central

Rain, Silvia; Andersen, Stine; Najafi, Aref; Gammelgaard Schultz, Jacob; da Silva Gonçalves Bós, Denielli; Handoko, M. Louis; Bogaard, Harm-Jan; Vonk-Noordegraaf, Anton; Andersen, Asger; van der Velden, Jolanda; Ottenheijm, Coen A.C.

2016-01-01

Background— The purpose of this study was to determine the relative contribution of fibrosis-mediated and myofibril-mediated stiffness in rats with mild and severe right ventricular (RV) dysfunction. Methods and Results— By performing pulmonary artery banding of different diameters for 7 weeks, mild RV dysfunction (Ø=0.6 mm) and severe RV dysfunction (Ø=0.5 mm) were induced in rats. The relative contribution of fibrosis- and myofibril-mediated RV stiffness was determined in RV trabecular strips. Total myocardial stiffness was increased in trabeculae from both mild and severe RV dysfunction in comparison to controls. In severe RV dysfunction, increased RV myocardial stiffness was explained by both increased fibrosis-mediated stiffness and increased myofibril-mediated stiffness, whereas in mild RV dysfunction, only myofibril-mediated stiffness was increased in comparison to control. Histological analyses revealed that RV fibrosis gradually increased with severity of RV dysfunction, whereas the ratio of collagen I/III expression was only elevated in severe RV dysfunction. Stiffness measurements in single membrane-permeabilized RV cardiomyocytes demonstrated a gradual increase in RV myofibril stiffness, which was partially restored by protein kinase A in both mild and severe RV dysfunction. Increased expression of compliant titin isoforms was observed only in mild RV dysfunction, whereas titin phosphorylation was reduced in both mild and severe RV dysfunction. Conclusions— RV myocardial stiffness is increased in rats with mild and severe RV dysfunction. In mild RV dysfunction, stiffness is mainly determined by increased myofibril stiffness. In severe RV dysfunction, both myofibril- and fibrosis-mediated stiffness contribute to increased RV myocardial stiffness. PMID:27370069

Influenza as a trigger for acute myocardial infarction or death from cardiovascular disease: a systematic review.

PubMed

Warren-Gash, Charlotte; Smeeth, Liam; Hayward, Andrew C

2009-10-01

Cardiac complications of influenza infection, such as myocarditis, are well recognised, but the role of influenza as a trigger of acute myocardial infarction is less clear. We did a systematic review of the evidence that influenza (including influenza-like illness and acute respiratory infection) triggers acute myocardial infarction or cardiovascular death. We examined the effectiveness of influenza vaccines at protecting against cardiac events and did a meta-analysis of data from randomised controlled trials. 42 publications describing 39 studies were identified. Many observational studies in different settings with a range of methods reported consistent associations between influenza and acute myocardial infarction. There was weaker evidence of an association with cardiovascular death. Two small randomised trials assessed the protection provided by influenza vaccine against cardiac events in people with existing cardiovascular disease. Whereas one trial found that influenza vaccination gave significant protection against cardiovascular death, the other trial was inconclusive. A pooled estimate from a random-effects model suggests a protective, though non-significant, effect (relative risk 0.51, 95% CI 0.15-1.76). We believe influenza vaccination should be encouraged wherever indicated, especially in people with existing cardiovascular disease, among whom there is often suboptimum vaccine uptake. Further evidence is needed on the effectiveness of influenza vaccines to reduce the risk of cardiac events in people without established vascular disease.

Ruling out acute myocardial infarction. A prospective multicenter validation of a 12-hour strategy for patients at low risk.

PubMed

Lee, T H; Juarez, G; Cook, E F; Weisberg, M C; Rouan, G W; Brand, D A; Goldman, L

1991-05-02

Although previous investigations have suggested that 24 hours is required to exclude acute myocardial infarction in patients who are admitted to a coronary care unit for the evaluation of acute chest pain, we hypothesized that a 12-hour period might be adequate for patients with a low probability of infarction at the time of admission. Using a Bayesian model, we developed a strategy to identify candidates for a shorter period of observation from an analysis of a derivation set of 976 patients with acute chest pain who were admitted to three teaching and four community hospitals. In the derivation set, patients whose clinical characteristics in the emergency room predicted a low (less than or equal to 7 percent) probability of myocardial infarction had only a 0.4 percent risk of infarction if they had neither abnormal levels of cardiac enzymes nor recurrent ischemic pain during the first 12 hours of hospitalization. In an independent testing set of 2684 patients from the seven hospitals, 957 admitted patients (36 percent) were classified as candidates for this 12-hour period of observation according to a previously published multivariate algorithm. Few of these patients were actually transferred from a monitored setting at 12 hours. Of the 771 candidates for a 12-hour period of observation who did not have enzyme abnormalities or recurrent pain during the first 12 hours, 4 (0.5 percent) were subsequently found to have acute myocardial infarction, and only 3 (0.4 percent) died after primary cardiac arrests, all of which occurred three to five days after admission. Rates of other major cardiovascular complications were low in the patients who might have been transferred from the coronary care unit after 12 hours with this strategy. In patients with a higher initial risk of infarction, the standard strategy of 24-hour observation identified all but 11 of 739 acute myocardial infarctions (1 percent). Emergency room clinical data can be used to identify a large subgroup

Myocardial perfusion imaging study of CO(2)-induced panic attack.

PubMed

Soares-Filho, Gastão L F; Machado, Sergio; Arias-Carrión, Oscar; Santulli, Gaetano; Mesquita, Claudio T; Cosci, Fiammetta; Silva, Adriana C; Nardi, Antonio E

2014-01-15

Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response. Copyright © 2014 Elsevier Inc. All rights reserved.

Functional CT assessment of extravascular contrast distribution volume and myocardial perfusion in acute myocardial infarction.

PubMed

So, Aaron; Wisenberg, Gerald; Teefy, Patrick; Yadegari, Andrew; Bagur, Rodrigo; Hadway, Jennifer; Morrison, Laura; MacDonald, Anna; Gaskin, Dave; Butler, John; Biernaski, Heather; Skanes, Stephanie; Park, Stella DohYeoun; Islam, Ali; Hsieh, Jiang; Lee, Ting-Yim

2018-04-26

In a pig model of acute myocardial infarction (AMI), we validated a functional computed tomography (CT) technique for concomitant assessment of myocardial edema and ischemia through extravscualar contrast distribution volume (ECDV) and myocardial perfusion (MP) measurements from a single dynamic imaging session using a single contrast bolus injection. In seven pigs, balloon catheter was used to occlude the distal left anterior descending artery for one hour followed by reperfusion. CT and cardiac magnetic resonance (CMR) imaging studies were acquired on 3 days and 12 ± 3 day post ischemic insult. In each CT study, 0.7 ml/kg of iodinated contrast was intravenously injected at 3-4 ml/s before dynamic contrast-enhanced (DCE) cardiac images were acquired with breath-hold using a 64-row CT scanner. DCE cardiac images were analyzed with a model-based deconvolution to generate ECDV and MP maps. ECDV as an imaging marker of edema was validated against CMR T2 weighted imaging in normal and infarcted myocardium delineated from ex-vivo histological staining. ECDV in infarcted myocardium was significantly higher (p < 0.05) than that in normal myocardium on both days post AMI and was in agreement with the findings of CMR T2 weighted imaging. MP was significantly lower (p < 0.05) in the infarcted region compared to normal on both days post AMI. This imaging technique can rapidly and simultaneously assess myocardial edema and ischemia through ECDV and MP measurements, and may be useful for delineation of salvageable tissue within at-risk myocardium to guide reperfusion therapy. Copyright © 2017. Published by Elsevier B.V.

Metabolic Syndrome is Associated With Higher Wall Motion Score and Larger Infarct Size After Acute Myocardial Infarction

PubMed Central

Hajsadeghi, Shokoufeh; Chitsazan, Mitra; Chitsazan, Mandana; Haghjoo, Majid; Babaali, Nima; Norouzzadeh, Zahra; Mohsenian, Maryam

2015-01-01

Background: Infarct size is an important surrogate end point for early and late mortality after acute myocardial infarction. Despite the high prevalence of metabolic syndrome in patients with atherosclerotic diseases, adequate data are still lacking regarding the extent of myocardial necrosis after acute myocardial infarction in these patients. Objectives: In the present study we aimed to compare myocardial infarction size in patients with metabolic syndrome to those without metabolic syndrome using peak CK-MB and cardiac troponin I (cTnI) at 72 hours after the onset of symptoms. Patients and Methods: One-hundred patients with metabolic syndrome (group I) and 100 control subjects without metabolic syndrome (group II) who experienced acute myocardial infarction were included in the study. Diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines published in 2001. Myocardial infarction size was compared between the two groups of patients using peak CK-MB and cTnI level in 72 hours after the onset of symptoms. Results: Peak CK-MB and cTnI in 72 hours were found to be significantly higher in patients with metabolic syndrome compared with control subjects (both P < 0.001). Patients with metabolic syndrome also had markedly higher wall motion abnormality at 72 hours after the onset of symptoms as assessed by echocardiographically-derived Wall Motion Score Index (WMSI) (P < 0.001). Moreover, statistically significant relationships were found between WMSI and peak CK-MB and also cTnI at 72 hours (Spearman's rho = 0.56, P < 0.001 and Spearman's rho = 0.5, P < 0.001; respectively). However, association between WMSI and left ventricular ejection fraction was insignificant (Spearman's rho = -0.05, P = 0.46). Conclusions: We showed that patients with metabolic syndrome have larger infarct size compared to control subjects. PMID:25789257

Emergence of dendritic cells in the myocardium after acute myocardial infarction - implications for inflammatory myocardial damage.

PubMed

Yilmaz, Atilla; Dietel, Barbara; Cicha, Iwona; Schubert, Katja; Hausmann, Roland; Daniel, Werner G; Garlichs, Christoph D; Stumpf, Christian

2010-03-01

Dendritic cells (DC) are crucial for T cell mediated immune responses. Recently, we observed a significant decrease in circulating myeloid DC precursors in patients with acute myocardial infarction (AMI). The aim of the present study was to investigate whether myeloid DC are present in infarcted myocardium. Myocardial specimens of 10 patients with AMI and 7 accident victims (controls) were collected after autopsy. In immunostainings the presence of DC (CD209(+), fascin(+)), T cells (CD3(+)), macrophages (CD68(+)), and HLA-DR expression was analyzed. Significantly higher numbers of CD209(+)-DC (97 vs. 44 cells/0.25 mm(2), p=0.03), fascin(+)-DC (54 vs. 8 cells/0.25 mm(2), p=0.02), T cells (27 vs. 6 cells/0.25 mm(2), p=0.02), and macrophages (44 vs. 6 cells/0.25 mm(2), p=0.01) associated with high HLA-DR expression were detected in infarcted myocardium. Frequent colocalizations of DC and T cells were observed. In occluded coronary arteries numerous DC, T cells, macrophages and high HLA-DR expression were found. We show that DC are present in infarcted myocardium after AMI. High HLA-DR expression and the colocalization with T cells suggest that they might trigger an immune response leading to further myocardial damage.

Assessment of Quality Indicators for Acute Myocardial Infarction in the FAST-MI (French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction) Registries.

PubMed

Schiele, François; Gale, Chris P; Simon, Tabassome; Fox, Keith A A; Bueno, Hector; Lettino, Maddalena; Tubaro, Marco; Puymirat, Etienne; Ferrières, Jean; Meneveau, Nicolas; Danchin, Nicolas

2017-06-01

The Acute Cardiovascular Care Association defined quality indicators (QIs) for the management of acute myocardial infarction. The application of these QIs to existing databases is appealing. It remains to be determined what the rates of implementation are, how the QIs are related to long-term survival, and whether quality categorization is possible. The QIs were extracted from the French nationwide registries French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 (n=3670) and FAST-MI 2010 (n=4169). Implementation rates for each QI are reported for both cohorts. The composite QI was used for benchmarking, and the relationship between QIs and 3-year survival was determined using a Cox model. In FAST-MI 2010, 12 individual and 2 composite QIs could be assessed. Four QIs were not recorded in FAST-MI 2010 and 4 in 2005, either because of treatment nonavailability or because of data not recorded. The degree of implementation ranged from 12% to 89%, with higher rates in 2010 as compared with 2005. Seven individual QIs were associated with survival, and there was a significant and gradual association between survival and categories of the composite QI. Center categorization was possible in 26% to 30% of participating centers; 16 (27%) centers in 2005 and 14 (20%) in 2010 were categorized as low quality. Twelve of 17 individual QIs could be assessed from FAST-MI 2010. The composite QI was significantly associated with 3-year survival and distinguished centers with high, average, and low quality of care. © 2017 American Heart Association, Inc.

Detection and differentiation of early acute and following age stages of myocardial infarction with quantitative post-mortem cardiac 1.5T MR.

PubMed

Schwendener, Nicole; Jackowski, Christian; Persson, Anders; Warntjes, Marcel J; Schuster, Frederick; Riva, Fabiano; Zech, Wolf-Dieter

2017-01-01

Recently, quantitative MR sequences have started being used in post-mortem imaging. The goal of the present study was to evaluate if early acute and following age stages of myocardial infarction can be detected and discerned by quantitative 1.5T post-mortem cardiac magnetic resonance (PMCMR) based on quantitative T1, T2 and PD values. In 80 deceased individuals (25 female, 55 male), a cardiac MR quantification sequence was performed prior to cardiac dissection at autopsy in a prospective study. Focal myocardial signal alterations detected in synthetically generated MR images were MR quantified for their T1, T2 and PD values. The locations of signal alteration measurements in PMCMR were targeted at autopsy heart dissection and cardiac tissue specimens were taken for histologic examinations. Quantified signal alterations in PMCMR were correlated to their according histologic age stage of myocardial infarction. In PMCMR seventy-three focal myocardial signal alterations were detected in 49 of 80 investigated hearts. These signal alterations were diagnosed histologically as early acute (n=39), acute (n=14), subacute (n=10) and chronic (n=10) age stages of myocardial infarction. Statistical analysis revealed that based on their quantitative T1, T2 and PD values, a significant difference between all defined age groups of myocardial infarction can be determined. It can be concluded that quantitative 1.5T PMCMR quantification based on quantitative T1, T2 and PD values is feasible for characterization and differentiation of early acute and following age stages of myocardial infarction. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

The role of a structured exercise training program on cardiac structure and function after acute myocardial infarction: study protocol for a randomized controlled trial.

PubMed

Fontes-Carvalho, Ricardo; Sampaio, Francisco; Teixeira, Madalena; Gama, Vasco; Leite-Moreira, Adelino F

2015-03-12

Exercise training is effective in improving functional capacity and quality of life in patients with coronary artery disease, but its effects on left ventricular systolic and diastolic function are controversial. Diastolic dysfunction is a major determinant of adverse outcome after myocardial infarction and, contrary to systolic function, no therapy or intervention has proved to significantly improve diastolic function. Data from animal studies and from patients with diastolic heart failure has suggested that exercise training can have a positive effect on diastolic function parameters. This trial aims to evaluate if a structured exercise training program can improve resting left ventricular diastolic and systolic function in patients who have had an acute myocardial infarction. This is a phase II, prospective, randomized, open-label, blinded-endpoint trial that will include at least 96 consecutive patients who have had an acute myocardial infarction one month previously. Patients will be randomized (1:1) to an exercise training program or a control group, receiving standard of care. At enrolment, and at the end of the follow-up period, patients will be submitted to an echocardiography (with detailed assessment of diastolic and systolic function using recent consensus guidelines), cardiopulmonary exercise testing, an anthropometric assessment, blood testing, and clinical evaluation. Patients randomized to the intervention group will be submitted to an eight-week outpatient exercise program, combining endurance and resistance training, for three sessions per week. The primary endpoint will be the change in lateral E' velocity immediately after the eight-week exercise training program. Secondary endpoints will include other echocardiographic parameters of left ventricular diastolic and systolic function, cardiac structure, metabolic and inflammation biomarkers (high-sensitivity C-reactive protein and pro-BNP), functional capacity (peak oxygen consumption and

Acute Myocardial Infarction from Coronary Vasospasm Precipitated by Pseudoephedrine and Metoprolol Use.

PubMed

Meoli, Elise M; Goldsweig, Andrew M; Malm, Brian J

2017-05-01

Pseudoephedrine is a sympathomimetic α- and β-adrenergic receptor agonist that causes vasoconstriction and reduction in edema throughout the nasal passages. Coronary vasospasm associated with pseudoephedrine has been reported in the literature. We discuss the case of a patient with new-onset atrial fibrillation receiving metoprolol for rate control on a background of pseudoephedrine use for allergic rhinitis leading to acute myocardial infarction from multivessel coronary vasospasm. This case illustrates the importance of understanding the pharmacology of potential drug-drug interactions when managing patients with acute cardiovascular syndromes. Published by Elsevier Inc.

Synthetic Marijuana Induced Acute Nonischemic Left Ventricular Dysfunction.

PubMed

Elsheshtawy, Moustafa; Sriganesh, Priatharsini; Virparia, Vasudev; Patel, Falgun; Khanna, Ashok

2016-01-01

Synthetic marijuana is an uptrending designer drug currently widely spread in the US. We report a case of acute deterioration of nonischemic left ventricular dysfunction after exposure to synthetic marijuana. This case illustrates the importance of history taking in cardiac patients and identifies a negative cardiovascular effect of synthetic marijuana known as K2, not yet well detected by urine toxicology screening tools.

Impaired left ventricular diastolic function is related to the formation of left ventricular apical thrombus in patients with acute anterior myocardial infarction.

PubMed

Choi, Ung Lim; Park, Jae-Hyeong; Sun, Byung Joo; Oh, Jin Kyung; Seong, Seok Woo; Lee, Jae-Hwan; Choi, Si Wan; Jeong, Jin-Ok; Kwon, In Sun; Seong, In-Whan

2018-05-01

Left ventricular (LV) apical thrombus is a clinically important complication which can cause systemic embolization in patients with anterior acute myocardial infarction (AMI). Systolic dysfunction has been a risk factor for developing LV apical thrombus in AMI patients. However, the role of diastolic dysfunction in the development of LV apical thrombus in these patients is still unknown. We performed this study to evaluate whether diastolic dysfunction can influence the development of LV apical thrombus in anterior AMI patients. We retrospectively analyzed all consecutive anterior AMI patients with available echocardiographic images within 1 month from January 2005 to April 2016. After gathering clinical characteristics from their medical records, systolic and diastolic functions were analyzed from digitally stored echocardiographic images. We included a total of 1045 patients (748 males, mean age 64 ± 12 years) with anterior AMI, and 494 (47%) were diagnosed as STEMI. The incidence of LV apical thrombus was 3.3% (34/1045). The LV apical thrombus group had larger LV diastolic dimension, larger LV diastolic and systolic volumes, and lower LVEF than the no LV thrombus group. The LV apical thrombus group showed higher mitral E velocity over mitral annular E' velocity ratio, an indicator of LV end-diastolic pressure (P < 0.001). In the LV apical thrombus group, the incidence of grade 2 diastolic dysfunction (32 vs 12%, P = 0.001) and grade 3 diastolic dysfunction (26 vs 2%, P < 0.001) were significantly higher than in the no LV apical thrombus group. The presence of more than grade 2 diastolic dysfunction, LVEF and presence of LV apical aneurysm were statistically significant factors associated with LV apical thrombus after the multivariate analysis. In conclusion, along with LV systolic dysfunction and LV apical aneurysm, LV diastolic dysfunction was also related with the presence of LV apical thrombus in patients with anterior AMI.

Regional heterogeneity in cardiac sympathetic innervation in acute myocardial infarction: relationship with myocardial oedema on magnetic resonance.

PubMed

Gimelli, Alessia; Masci, Pier Giorgio; Liga, Riccardo; Grigoratos, Chrysanthos; Pasanisi, Emilio Maria; Lombardi, Massimo; Marzullo, Paolo

2014-09-01

To assess the relationships between myocardial structure and function on cardiac magnetic resonance (CMR) imaging and sympathetic tone on (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy early after myocardial infarction (MI). Ten patients underwent (123)I-MIBG and (99m)Tc-tetrofosmin rest cadmium zinc telluride scintigraphy 4 ± 1 days after MI. The segmental left ventricular (LV) relative radiotracer uptake of both (99m)Tc-tetrofosmin and early (123)I-MIBG was calculated. The day after scintigraphy, on CMR imaging, the extent of ischaemia-related oedema and of myocardial fibrosis (late gadolinium enhancement, LGE) was assessed. Accordingly, the extent of oedema and LGE was evaluated for each segment and segmental wall thickening determined. Based on LGE distribution, LV segments were categorized as "infarcted" (56 segments), "adjacent" (66 segments) or "remote" (48 segments). Infarcted segments showed a more depressed systolic wall thickening and greater extent of oedema than adjacent segments (p < 0.001) and remote segments (p < 0.001). Interestingly, while uptake of (99m)Tc-tetrofosmin was significantly depressed only in infarcted segments (p < 0.001 vs. both adjacent and remote segments), uptake of (123)I-MIBG was impaired not only in infarcted segments (p < 0.001 vs. remote) but also in adjacent segments (p = 0.024 vs. remote segments). At the regional level, after correction for (99m)Tc-tetrofosmin and LGE distribution, segmental (123)I-MIBG uptake (p < 0.001) remained an independent predictor of ischaemia-related oedema. After acute MI the regional impairment of sympathetic tone extends beyond the area of altered myocardial perfusion and is associated with myocardial oedema.

Sibutramine-induced acute myocardial infarction in a young lady.

PubMed

Yim, Kin-Ming Anfernee; Ng, Hon Wah; Chan, Chi-Kin; Yip, Gabriel; Lau, Fei Lung

2008-11-01

Sibutramine is an amphetamine-like drug used for its weight reducing effect. Sibutramine-induced acute coronary syndrome has rarely been reported. We report a case of myocardial infarction associated with the use of sibutramine. A 37-year-old woman presented to an Emergency Department (ED) with intermittent retrosternal chest pain, nausea, and sweating for 3 days. She reported taking one sibutramine tablet each day for 3 days. Blood pressure was 128/89 mm Hg and pulse 66 beats/min. An electrocardiogram revealed ST elevation over the inferior leads and ST depression over leads AVR and V1, the other leads were normal. Serum troponin T was 0.65 microg/L, and sibutramine was identified in her urine. Echocardiography revealed mild hypokinesia over the inferior wall without evidence of acute aortic dissection. The ST segment changes resolved spontaneously within 24 h of cardiac care unit (CCU) admission, a coronary angiogram performed 1 week later was unremarkable, and echocardiography performed 4 weeks after the event showed normal resting regional wall motion. Seventeen medications containing sibutramine as an active ingredient were registered in Hong Kong in 2007. Sibutramine was introduced in the United States in 1997 and in Australia, United Kingdom, and Italy in 2001. Hypertension, tachycardia, dry mouth, and headache are the most commonly reported adverse reactions. Cardiovascular toxicities include tachycardia, palpitation, hypertension, and tachyarrhythmia. We postulate that the myocardial infarction was the result of coronary vasospasm associated with the therapeutic use of sibutramine-containing slimming pills.

Sex Differences in Trajectories of Risk After Rehospitalization for Heart Failure, Acute Myocardial Infarction, or Pneumonia.

PubMed

Dreyer, Rachel P; Dharmarajan, Kumar; Hsieh, Angela F; Welsh, John; Qin, Li; Krumholz, Harlan M

2017-05-01

Women have an increased risk of rehospitalization in the immediate postdischarge period; however, few studies have determined how readmission risk dynamically changes on a day-to-day basis over the full year after hospitalization by sex and how these differences compare with the risk for mortality. We identified >3 000 000 hospitalizations of patients with a principal discharge diagnosis of heart failure, acute myocardial infarction, or pneumonia and estimated sex differences in the daily risk of rehospitalization/death 1 year after discharge from a population of Medicare fee-for-service beneficiaries aged 65 years and older. We calculated the (1) time required for adjusted rehospitalization/mortality risks to decline 50% from maximum values after discharge, (2) time required for the adjusted readmission risk to approach plateau periods of minimal day-to-day change, and (3) extent to which adjusted risks are greater among recently hospitalized patients versus Medicare patients. We identified 1 392 289, 530 771, and 1 125 231 hospitalizations for heart failure, acute myocardial infarction, and pneumonia, respectively. The adjusted daily risk of rehospitalization varied by admitting condition (hazard rate ratio for women versus men, 1.10 for acute myocardial infarction; hazard rate ratio, 1.04 for heart failure; and hazard rate ratio, 0.98 for pneumonia). However, for all conditions, the adjusted daily risk of death was higher among men versus women (hazard rate ratio women versus with men, <1). For both sexes, there was a similar timing of peak daily risk, half daily risk, and reaching plateau. Although the association of sex with daily risk of rehospitalization varies across conditions, women are at highest risk after discharge for acute myocardial infarction. Future studies should focus on understanding the determinants of sex differences in rehospitalization risk among conditions. © 2017 American Heart Association, Inc.

Overweight female rats selectively breed for low aerobic capacity exhibit increased myocardial fibrosis and diastolic dysfunction

PubMed Central

Johnson, Megan S.; Ma, Lixin; Pulakat, Lakshmi; Mugerfeld, Irina; Hayden, Melvin R.; Garro, Mona; Knight, William; Britton, Steven L.; Koch, Lauren G.; Sowers, James R.

2012-01-01

The statistical association between endurance exercise capacity and cardiovascular disease suggests that impaired aerobic metabolism underlies the cardiovascular disease risk in men and women. To explore this connection, we applied divergent artificial selection in rats to develop low-capacity runner (LCR) and high-capacity runner (HCR) rats and found that disease risks segregated strongly with low running capacity. Here, we tested if inborn low aerobic capacity promotes differential sex-related cardiovascular effects. Compared with HCR males (HCR-M), LCR males (LCR-M) were overweight by 34% and had heavier retroperitoneal, epididymal, and omental fat pads; LCR females (LCR-F) were 20% heavier than HCR females (HCR-F), and their retroperitoneal, but not perireproductive or omental, fat pads were heavier as well. Unlike HCR-M, blood pressure was elevated in LCR-M, and this was accompanied by left ventricular (LV) hypertrophy. Like HCR-F, LCR-F exhibited normal blood pressure and LV weight as well as increased spontaneous cage activity compared with males. Despite normal blood pressures, LCR-F exhibited increased myocardial interstitial fibrosis and diastolic dysfunction, as indicated by increased LV stiffness, a decrease in the initial filling rate, and an increase in diastolic relaxation time. Although females exhibited increased arterial stiffness, ejection fraction was normal. Increased interstitial fibrosis and diastolic dysfunction in LCR-F was accompanied by the lowest protein levels of phosphorylated AMP-actived protein kinase [phospho-AMPK (Thr172)] and silent information regulator 1. Thus, the combination of risk factors, including female sex, intrinsic low aerobic capacity, and overweightness, promote myocardial stiffness/fibrosis sufficient to induce diastolic dysfunction in the absence of hypertension and LV hypertrophy. PMID:22345570

Methamphetamine-associated acute myocardial infarction and cardiogenic shock with normal coronary arteries: refractory global coronary microvascular spasm.

PubMed

Chen, Jack P

2007-04-01

Methamphetamine (MET) is a growing public health concern and is prevalent in, although not limited to, the youth. The drug's association with myocardial infarction is well described and is attributed to accelerated atherosclerosis, hypercoagulable state, and macrovascular epicardial coronary spasm. However, global slow-flow of all coronary systems in the absence of significant stenoses has not been previously reported. We hereby present a young patient who likely experienced severe, global microvascular coronary spasm unrelieved by intracoronary vasodilator therapy, resulting in acute myocardial infarction. The pharmacology of MET, its postulated mechanism in acute coronary syndromes, as well as the pathophysiology and treatments of microvascular coronary spasm are briefly reviewed. Readers are recommended to be vigilant of potential illicit drug use in patients with atypical presentations of acute coronary syndromes.

Comparison of case fatality in south Asian and white patients after acute myocardial infarction: observational study.

PubMed

Wilkinson, P; Sayer, J; Laji, K; Grundy, C; Marchant, B; Kopelman, P; Timmis, A D

1996-05-25

To compare mortality in south Asian (Indian, Pakistani, and Bangladeshi) and white patients in the six months after hospital admission for acute myocardial infarction. Observational study. District general hospital in east London. 149 south Asian and 313 white patients aged < 65 years admitted to the coronary care unit with acute myocardial infarction from 1 December 1988 to 31 December 1992. All cause mortality in the first six months after myocardial infarction. The admission rate in the south Asians was estimated to be 2.04 times that in the white patients. Most aspects of treatment were similar in the two groups, except that a higher proportion of the south Asians received thrombolytic drugs (81.2% v 73.8%). After adjustment for age, sex, previous myocardial infarction, and treatment with thrombolysis or aspirin, or both, the south Asians had a poorer survival over the six months from myocardial infarction (hazard ratio 2.02 (95% confidence interval 1.14 to 3.56), P = 0.018), but a substantially higher proportion were diabetic (38% v 11%, P < 0.001), and additional adjustment for diabetes removed much of their excess risk (adjusted hazard ratio 1.26 (0.68 to 2.33), P = 0.47). South Asian patients had a higher risk of admission with myocardial infarction and a higher risk of death over the ensuing six months than the white patients. The higher case fatality among the south Asians, largely attributable to diabetes, may contribute to the increased risk of death from coronary heart disease in south Asians living in Britain.

Oxygen therapy for acute myocardial infarction.

PubMed

Cabello, Juan B; Burls, Amanda; Emparanza, José I; Bayliss, Susan E; Quinn, Tom

2016-12-19

Oxygen (O 2 ) is widely used in people with acute myocardial infarction (AMI). Previous systematic reviews concluded that there was insufficient evidence to know whether oxygen reduced, increased or had no effect on heart ischaemia or infarct size. Our first Cochrane review in 2010 also concluded there was insufficient evidence to know whether oxygen should be used. Since 2010, the lack of evidence to support this widely used intervention has attracted considerable attention, prompting further trials of oxygen therapy in myocardial infarction patients. It is thus important to update this Cochrane review. To assess the effects of routine use of inhaled oxygen for acute myocardial infarction (AMI). We searched the following bibliographic databases on 6 June 2015: the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE (OVID), Embase (OVID), CINAHL (EBSCO) and Web of Science (Thomson Reuters). LILACS (Latin American and Caribbean Health Sciences Literature) was last searched in September 2016. We also contacted experts to identify eligible studies. We applied no language restrictions. Randomised controlled trials in people with suspected or proven AMI (ST-segment elevation myocardial infarction (STEMI) or non-STEMI) within 24 hours after onset, in which the intervention was inhaled oxygen (at normal pressure) compared to air, regardless of co-therapies provided to participants in both arms of the trial. Two authors independently reviewed the titles and abstracts of identified studies to see if they met the inclusion criteria and independently undertook the data extraction. We assessed the quality of studies and the risk of bias according to guidance in the Cochrane Handbook for Systematic Reviews of Interventions. The primary outcome was death. The measure of effect used was the risk ratio (RR) with a 95% confidence interval (CI). We used the GRADE approach to evaluate the quality of the evidence and the GRADE profiler (GRADEpro

Potential cost effectiveness of intravenous tissue plasminogen activator versus streptokinase for acute myocardial infarction.

PubMed

Goel, V; Naylor, C D

1992-01-01

An economic evaluation of the potential incremental benefits of intravenous tissue plasminogen activator (tPA) versus streptokinase (SK) for treatment of acute myocardial infarction. Cost effectiveness analysis from a third-party payer perspective (Ontario Ministry of Health). ECONOMIC INPUTS: Fully allocated costs for cardiovascular procedures and hospitalization for myocardial infarction were obtained anonymously for four Ontario teaching hospitals and converted to 1988 Canadian dollars. Professional charges were taken from the provincial health insurance fee schedule and drug costs obtained from the manufacturers. CLINICAL INPUTS: The baseline analysis was for nonelderly patients with uncomplicated myocardial infarctions; sensitivity analyses allowed extrapolation to higher risk subgroups. Short and longer term mortality and short term invasive procedure rates were estimated using data from clinical trials. If tPA achieves a 1% short term mortality advantage over SK with no advantages for other survivors, cost per life-year gained can be comparable to other cardiovascular interventions at $58,600. In the absence of immediate survival advantages, but assuming greater left ventricular preservation, the constant annual hazard rate advantage must be about 0.5% per year for competitive cost effectiveness ratios. A full range of projections is presented to help guide the policy decisions that will arise in the wake of the Global Utilization of SK and tPA for Occluded Coronary Arteries (GUSTO) trial. The analysis also illustrates the general importance of considering longer term effects of in-hospital therapies for acute myocardial infarction.

The amelioration of cardiac dysfunction after myocardial infarction by the injection of keratin biomaterials derived from human hair.

PubMed

Shen, Deliang; Wang, Xiaofang; Zhang, Li; Zhao, Xiaoyan; Li, Jingyi; Cheng, Ke; Zhang, Jinying

2011-12-01

Cardiac dysfunction following acute myocardial infarction is a major cause of advanced cardiomyopathy. Conventional pharmacological therapies rely on prompt reperfusion and prevention of repetitive maladaptive pathways. Keratin biomaterials can be manufactured in an autologous fashion and are effective in various models of tissue regeneration. However, its potential application in cardiac regeneration has not been tested. Keratin biomaterials were derived from human hair and its structure morphology, carryover of beneficial factors, biocompatibility with cardiomyocytes, and in vivo degradation profile were characterized. After delivery into infarcted rat hearts, the keratin scaffolds were efficiently infiltrated by cardiomyocytes and endothelial cells. Injection of keratin biomaterials promotes angiogenesis but does not exacerbate inflammation in the post-MI hearts. Compared to control-injected animals, keratin biomaterials-injected animals exhibited preservation of cardiac function and attenuation of adverse ventricular remodeling over the 8 week following time course. Tissue western blot analysis revealed up-regulation of beneficial factors (BMP4, NGF, TGF-beta) in the keratin-injected hearts. The salient functional benefits, the simplicity of manufacturing and the potentially autologous nature of this biomaterial provide impetus for further translation to the clinic. Copyright © 2011 Elsevier Ltd. All rights reserved.

Remote ischaemic postconditioning protects the heart during acute myocardial infarction in pigs.

PubMed

Andreka, Gyorgy; Vertesaljai, Marton; Szantho, Gergely; Font, Gusztav; Piroth, Zsolt; Fontos, Geza; Juhasz, Eszter D; Szekely, Laszlo; Szelid, Zsolt; Turner, Mark S; Ashrafian, Houman; Frenneaux, Michael P; Andreka, Peter

2007-06-01

Ischaemic preconditioning results in a reduction in ischaemic-reperfusion injury to the heart. This beneficial effect is seen both with direct local preconditioning of the myocardium and with remote preconditioning of easily accessible distant non-vital limb tissue. Ischaemic postconditioning with a comparable sequence of brief periods of local ischaemia, when applied immediately after the ischaemic insult, confers benefits similar to preconditioning. To test the hypothesis that limb ischaemia induces remote postconditioning and hence reduces experimental myocardial infarct size in a validated swine model of acute myocardial infarction. Acute myocardial infarction was induced in 24 pigs with 90 min balloon inflations of the left anterior descending coronary artery. Remote ischaemic postconditioning was induced in 12 of the pigs by four 5 min cycles of blood pressure cuff inflation applied to the lower limb immediately after the balloon deflation. Infarct size was assessed by measuring 72 h creatinine kinase release, MRI scan and immunohistochemical analysis. Area under the curve of creatinine kinase release was significantly reduced in the postconditioning group compared with the control group with a 26% reduction in the infarct size (p<0.05). This was confirmed by MRI scanning and immunohistochemical analysis that revealed a 22% (p<0.05) and a 47.52% (p<0.01) relative reduction in the infarct size, respectively. Remote ischaemic postconditioning is a simple technique to reduce infarct size without the hazards and logistics of multiple coronary artery balloon inflations. This type of conditioning promises clear clinical potential.

Protection of Distal Embolization in High-Risk Patients with Acute ST-Segment Elevation Myocardial Infarction (PREMIAR).

PubMed

Cura, Fernando A; Escudero, Alejandro Garcia; Berrocal, Daniel; Mendiz, Oscar; Trivi, Marcelo S; Fernandez, Juan; Palacios, Alejandro; Albertal, Mariano; Piraino, Ruben; Riccitelli, Miguel Angel; Gruberg, Luis; Ballarino, Miguel; Milei, Jose; Baeza, Ricardo; Thierer, Jorge; Grinfeld, Liliana; Krucoff, Mitchell; O'Neill, William; Belardi, Jorge

2007-02-01

Distal embolization may decrease myocardial reperfusion after primary percutaneous coronary intervention (PCI). Nonetheless, results of previous trials assessing the role of distal protection during primary PCI have been controversial. The Protection of Distal Embolization in High-Risk Patients with Acute ST-Segment Elevation Myocardial Infarction Trial (PREMIAR) was a prospective, randomized, controlled study designed to evaluate the role of filter-based distal protection during PCI in patients with acute ST-segment elevation myocardial infarction at high risk of embolic events (including only baseline Thrombolysis In Myocardial Infarction grade 0 to 2 flow). The primary end point was continuous monitoring of ST-segment resolution. Secondary end points included core laboratory analysis of angiographic myocardial blush, ejection fraction measured by cardiac ultrasound, and adverse cardiac events at 6 months. From a total of 194 enrolled patients, 140 subjects were randomized to PCI with or without embolic protection, and 54 were included in a registry arm due to the presence of angiographic exclusion criteria. Baseline characteristics were comparable between arms. The rate of complete ST-segment resolution (>or=70%) at 60 minutes was similar in patients treated with or without distal protection (61.2% vs 60.3%, respectively, p = 0.85). Angiographic myocardial blush (67% vs 70.7%, p = 0.73), in-hospital ejection fraction (47.4 +/- 9.9% vs 45.3 +/- 7.3%, p = 0.29), and combined end point of death, heart failure, or reinfarction at 6 months (14.3% vs 15.7%, p = 0.81) were consistently achieved in a similar proportion in the 2 groups. In conclusion, the use of filter-based distal protection is safe and effectively retrieves debris; however, such use does not translate into an improvement of myocardial reperfusion, left ventricular performance, or clinical outcomes.

Ultrasound imaging of propagation of myocardial contraction for non-invasive identification of myocardial ischemia

NASA Astrophysics Data System (ADS)

Matsuno, Yuya; Taki, Hirofumi; Yamamoto, Hiroaki; Hirano, Michinori; Morosawa, Susumu; Shimokawa, Hiroaki; Kanai, Hiroshi

2017-07-01

Non-invasive identification of ischemic regions is important for diagnosis and treatment of myocardial infarction. In the present study, ultrasound measurement was applied to the interventricular septum of three open-chest swine hearts. The properties of the myocardial contraction response of the septum were compared between normal and acute ischemic conditions, where the acute ischemic condition of the septum originated from direct avascularization of the left anterior descending (LAD) coronary artery. The result showed that the contraction response propagated from the basal side to the apical side along the septum. The estimated propagation velocities in the normal and acute ischemic conditions were 3.6 and 1.9 m/s, respectively. This finding indicates that acute ischemia which occurred 5 s after the avascularization of the LAD promptly suppressed the propagation velocity through the ventricular septum to about half the normal velocity. It was suggested that the myocardial ischemic region could be identified using the difference in the propagation velocity of the myocardial response to contraction.

Prevalence of arterial stiffness and the risk of myocardial diastolic dysfunction in women.

PubMed

Seeland, Ute; Brecht, Anna; Nauman, Ahmad T; Oertelt-Prigione, Sabine; Ruecke, Mirjam; Knebel, Fabian; Stangl, Verena; Regitz-Zagrosek, Vera

2016-10-01

The present study determines the prevalence of vascular dysfunction and arterial stiffness (ASt) in a female urban population by measuring the brachial augmentation index (AIx) and aortic pulse wave velocity (PWV). The study tests the hypothesis that the measurement of AIx and PWV is useful in addition to that of traditional cardiovascular risk factors when assessing the risk for left ventricular diastolic dysfunction (LVDD). This cross-sectional study recruited 965 women aged 25-75 years from 12 districts of Berlin. The ASt indices, brachial AIx, aortic PWV and the central blood pressure were measured by an oscillometric method. A randomly selected subgroup (n=343) was examined by echocardiography. Trans-mitral inflow E/A ratio and diastolic mitral annulus velocity (é) were assessed. Questionnaires, medical history and blood sampling were used for the evaluation of individual risk factors. Normal vascular function was found in 55% of the women included. The prevalence of women with pathological AIx only (AIx ⩾ -10%, PWV normal) was 21.5%, whereas 17.9% were affected by increased AIx and PWV (AIx ⩾ -10%, PWV ⩾9.7 m/s), and 6% with only pathological PWV values. The prevalence of LVDD was 31.7%. LVDD was significantly associated with pathological PWV ⩾ 9.7 m/s [OR: 1.27, 95%CI: 1.02-1.57], age [OR: 4.17, 95%CI: 2.87-6.07] and a waist circumference >80 cm [OR: 3.61, 95%CI: 1.85-7.04] in multiple regression analysis. The high prevalence of markers for vascular dysfunction and ASt in a general female population and their importance as a mediator of diastolic dysfunction should encourage implementation of aortic PWV measurement to improve cardiovascular-risk assessment in particular to identify subclinical myocardial diastolic dysfunction. © 2016 The Author(s).

Mechanisms of acute myocardial infarction study (MAMIS).

PubMed

Singh, Ram B; Pella, Daniel; Neki, Nirankar S; Chandel, J P; Rastogi, Saurabh; Mori, Heideki; Otsuka, Kuniaki; Gupta, Pankaj

2004-10-01

Acute myocardial infarction (AMI) is a highly dynamic event, which is associated with marked neuroendocrinological dysfunction in addition to cardiac damage. The immediate trigger for AMI is not precisely known. Studies conducted by Lown, Braunwald, Halberg, Otsuka and our group have demonstrated a marked increase in sympathetic activity, oxidative stress, and magnesium and potassium deficiency during AMI. Clinical studies have reported an increased incidence of AMI, sudden death and ischemia during first quarter of the day when there is a rapid withdrawal of vagal activity and increase in sympathetic tone. In one case-control study of 202 patients with AMI, there was a significant (P < 0.02) increase in cardiac events in the second quarter of the day compared to other quarters, respectively (16.8%, 41.0%, 13.8%, 28.2% per quarter). This characteristic remained prevalent in both men and women and among patients with and without known AMI (n = 52), diabetes (n = 53) or hypertension (n = 75). Triggers of AMI were noted among 162 (82.2%) of the patients. Neuropsychological mechanisms were observed as follows: emotional stress (45.5%), sleep deprivation (27.7%), cold climate (29.2%), hot climate (24.7%), large meals (47.5%) and physical exertion (31.2%). These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting in an increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotension-converting enzyme (ACE), interleukin (IL)-1, -2, -6, -18, and tumor necrosis factor-alpha (TNF-alpha), all of which are are proinflammatory agents. There is also a deficiency in the serum levels of vitamin A, E, and C and magnesium, potassium, melatonin, and IL-10 (an anti-inflammatory agent). In our study, we found a decrease in magnesium, potassium, vitamin A, E, C and beta carotene combined with an increase in thiobarbituric acid-reactive substances (TBARS), MDA and diene conjugates, TNF-alpha and IL-6, all of which are indicators

Mortality and Revascularization following Admission for Acute Myocardial Infarction: Implication for Rural Veterans

ERIC Educational Resources Information Center

Abrams, Thad E.; Vaughan-Sarrazin, Mary; Kaboli, Peter J.

2010-01-01

Introduction: Annually, over 3,000 rural veterans are admitted to Veterans Health Administration (VA) hospitals for acute myocardial infarction (AMI), yet no studies of AMI have utilized the VA rural definition. Methods: This retrospective cohort study identified 15,870 patients admitted for AMI to all VA hospitals. Rural residence was identified…

Effect of milrinone on short term outcome of patients with myocardial dysfunction undergoing off-pump coronary artery bypass graft: a randomized clinical trial.

PubMed

Hadadzadeh, Mehdi; Hosseini, Seyed Habib; Mostafavi Pour Manshadi, Seyed Mohammad Yousof; Naderi, Nafiseh; Emami Meybodi, Mahmood

2013-01-01

Myocardial dysfunction is a major complication in cardiac surgery that needs inotropic support. This study evaluates the effect of milrinone on patients with low ventricular ejection fraction undergoing off- pump coronary artery bypass graft (OPCAB). The present study is designed to evaluate the effect of milrinone on myocardial dysfunction. Eighty patients with low ventricular ejection fraction (<35%), candidate for elective OPCAB, were enrolled in this study. They were randomly assigned to two groups. One group received milrinone (50 μg/kg) intravenously and another group received a saline as placebo followed by 24 hours infusion of each agent (0.5 μg/kg/min). Short outcome of patients such as hemodynamic parameters and left ventricular ejection fraction were variables evaluated. Serum levels of creatine phosphokinase, the MB isoenzyme of creatine kinase, occurrence of arrhythmias and mean duration of mechanical ventilation were significantly lower in milrinone group (P<0.05). The mean post operative left ventricular ejection fraction was significantly higher in milrinone group (P=0.031). There were no statistical significant differences between the two groups in terms of intra-aortic balloon pump, inotropic support requirement, myocardial ischemia, myocardial infarction, duration of inotropic support, duration of intensive care unit stay, mortality and morbidity rate. Administration of milrinone in patients undergoing OPCAB with low ventricular ejection fraction is useful and effective.

Electrocardiographic evaluation of reperfusion therapy in patients with acute myocardial infarction.

PubMed

Clemmensen, P

1996-02-01

The present thesis is based on 6 previously published clinical studies in patients with AMI. Thrombolytic therapy for patients with AMI improves early infarct coronary artery patency, limits AMI size, improves left ventricular function and survival, as demonstrated in large placebo-controlled clinical trials. With the advent of interventions aimed at limiting AMI size it became important to assess the amount of ischemic myocardium in the early phase of AMI, and to develop noninvasive methods for evaluation of these therapies. The aims of the present studies were to develop such methods. The studies have included 267 patients with AMI admitted up to 12 hours after onset of symptoms. All included patients had acute ECG ST-segment changes indicating subepicardial ischemia, and patients with bundle branch block were excluded. Serial ECG's were analyzed with quantitative ST-segment measurements in the acute phase and compared to the Selvester QRS score estimated final AMI size. These ECG indices were compared to and validated through comparisons with other independent noninvasive and invasive methods, used for the purpose of evaluating patients with AMI treated with thrombolytic therapy. It was found that in patients with first AMI not treated with reperfusion therapies the QRS score estimated final AMI size can be predicted from the acute ST-segment elevation. Based on the number of ECG leads with ST-segment elevation and its summated magnitude, formulas were developed to provide an "ST score" for estimating the amount of myocardium in jeopardy during the early phase of AMI. The ST-segment deviation present in the ECG in patients with documented occlusion of the infarct related coronary artery, was subsequently shown to correlate with the degree of regional and global left ventricular dysfunction. Because serial changes in ST-segment elevation, during the acute phase of AMI were believed to reflect changes is myocardial ischemia and thus possibly infarct artery patency

Risk of acute myocardial infarction after the death of a significant person in one's life: the Determinants of Myocardial Infarction Onset Study.

PubMed

Mostofsky, Elizabeth; Maclure, Malcolm; Sherwood, Jane B; Tofler, Geoffrey H; Muller, James E; Mittleman, Murray A

2012-01-24

Acute psychological stress is associated with an abrupt increase in the risk of cardiovascular events. Intense grief in the days after the death of a significant person may trigger the onset of acute myocardial infarction (MI), but this relationship has not been systematically studied. We conducted a case-crossover analysis of 1985 participants from the multicenter Determinants of Myocardial Infarction Onset Study interviewed during index hospitalization for an acute MI between 1989 and 1994. We compared the observed number of deaths in the days preceding MI symptom onset with its expected frequency based on each patient's control information, defined as the occurrence of deaths in the period from 1 to 6 months before infarction. Among the 1985 subjects, 270 (13.6%) experienced the loss of a significant person in the prior 6 months, including 19 within 1 day of their MI. The incidence rate of acute MI onset was elevated 21.1-fold (95% confidence interval, 13.1-34.1) within 24 hours of the death of a significant person and declined steadily on each subsequent day. The absolute risk of MI within 1 week of the death of a significant person is 1 excess MI per 1394 exposed individuals at low (5%) 10-year MI risk and 1 per 320 among individuals at high (20%) 10-year risk. Grief over the death of a significant person was associated with an acutely increased risk of MI in the subsequent days. The impact may be greatest among individuals at high cardiovascular risk.

Remote ischemic preconditioning and endothelial function in patients with acute myocardial infarction and primary PCI.

PubMed

Manchurov, Vladimir; Ryazankina, Nadezda; Khmara, Tatyana; Skrypnik, Dmitry; Reztsov, Roman; Vasilieva, Elena; Shpektor, Alexander

2014-07-01

Remote ischemic preconditioning by transient limb ischemia reduces myocardial ischemia-reperfusion injury in patients undergoing percutaneous coronary intervention. The aim of the study we report here was to assess the effect of remote ischemic preconditioning on endothelial function in patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Forty-eight patients with acute myocardial infarction were enrolled. All participants were randomly divided into 2 groups. In Group I (n = 23), remote ischemic preconditioning was performed before primary percutaneous coronary intervention (intermittent arm ischemia-reperfusion through 4 cycles of 5-minute inflation and 5-minute deflation of a blood-pressure cuff to 200 mm Hg). In Group II (n = 25), standard percutaneous coronary intervention without preconditioning was performed. We assessed endothelial function using the flow-mediated dilation test on baseline, then within 1-3 hours after percutaneous coronary intervention, and again on days 2 and 7 after percutaneous coronary intervention. The brachial artery flow-mediated dilation results were significantly higher on the first day after primary percutaneous coronary intervention in the preconditioning group (Group I) than in the control group (Group II) (12.1% vs 0.0%, P = .03, and 11.1% vs 6.3%, P = .016, respectively), and this difference remained on the seventh day (12.3% vs 7.4%, P = .0005, respectively). We demonstrated for the first time that remote ischemic preconditioning before primary percutaneous coronary intervention significantly improves endothelial function in patients with acute myocardial infarction, and this effect remains constant for at least a week. We suppose that the improvement of endothelial function may be one of the possible explanations of the effect of remote ischemic preconditioning. Copyright © 2014 Elsevier Inc. All rights reserved.

Effect of Early Statin Treatment in Patients with Cardiogenic Shock Complicating Acute Myocardial Infarction

PubMed Central

Sim, Doo Sun; Cho, Kyung Hoon; Ahn, Youngkeun; Kim, Young Jo; Chae, Shung Chull; Hong, Taek Jong; Seong, In Whan; Chae, Jei Keon; Kim, Chong Jin; Cho, Myeong Chan; Rha, Seung-Woon; Bae, Jang Ho; Seung, Ki Bae; Park, Seung Jung

2013-01-01

Background and Objectives The benefit of early statin treatment following acute myocardial infarction (MI) complicated with cardiogenic shock (CS) has not been well studied. We sought to assess the effect of early statin therapy in patients with CS complicating acute MI. Subjects and Methods We studied 553 statin-naive patients with acute MI and CS (Killip class IV) who underwent revascularization therapy between November 2005 and January 2008 at 51 hospitals in the Korea Acute Myocardial Infarction Registry. Patients were divided into 2 groups: those who received statins during hospitalization (n=280) and those who did not (n=273). The influence of statin treatment on a 12-month clinical outcome was examined using a matched-pairs analysis (n=200 in each group) based on the propensity for receiving statin therapy during hospitalization. Results Before adjustment, patients receiving statin, compared to those not receiving statin, had a more favorable clinical profile, were less likely to suffer procedural complications, and more likely to receive adequate medical therapy. Patients receiving statin had lower unadjusted in-hospital mortality and composite rate of mortality, MI, and repeat revascularization at 12 months, which remained significantly lower after adjustment for patient risk, procedural characteristics, and treatment propensity. Conclusion In CS patients with acute MI undergoing revascularization therapy, early statin treatment initiated during hospitalization was associated with lower rates of in-hospital death and 12-month adverse cardiac events. PMID:23508129

Transradial primary angioplasty and stenting in Indian patients with acute myocardial infarction: acute results and 6-month follow-up.

PubMed

Ranjan, Alok; Patel, Tejas M; Shah, Sanjay C; Malhotra, Hemant; Patel, Rajni; Vayada, Nishith; Pothiwala, Rasesh; Fonseca, Keith; Tanwar, Narendra S

2005-01-01

Coronary angioplasty and stent implantation is effective as primary intervention in acute myocardial infarction. Because of fewer puncture site complications and improved patient comfort, transradial access has been increasingly used as an alternative to transfemoral access for percutaneous coronary interventions. We studied 103 patients (94 men, 9 women: mean age 52.5 +/- 11.96 years) with a diagnosis of acute myocardial infarction (<12 hours after onset), who underwent primary percutaneous coronary intervention. Transradial access was used in all patients with a normal Allen's test and transfemoral access was used additionally only if intra-aortic balloon counterpulsation was required. Follow-up duration was 6 months. Transradial access was successfully achieved in all patients. Radial artery cannulation took <2 min in more than 85% patients. During percutaneous coronary intervention, cannulation to balloon inflation times and total procedure times were 11.3 +/- 5.2 min and 19.9 +/- 10.8 min, respectively. Stents were implanted in 99 (96.1%) patients andplain balloon angioplastywas performed in 3.9%. The primary success rate was 98.1%, with no major bleeding complications. Total length of hospitalization averaged 2.4 +/- 0.8 days. In-hospital major adverse clinical events rate was 5.9%. Six-month clinical follow-up was achieved for 84 (86.6%) patients. Six (7.1%) patients died during follow-up. Follow-up coronary angiography was performed in 22 (26.2%) patients. After 6 months, 7 patients required revascularizationof the target lesion. The rate of survival without myocardial infarction, bypass surgery or repeat coronary angioplasty was 88.5% at 6 months. Transradial access may represent a safe and feasible technique for performing primary percutaneous coronary intervention with good acute results and without major bleeding complications.

Lay Public's Knowledge and Decisions in Response to Symptoms of Acute Myocardial Infarction

ERIC Educational Resources Information Center

Cytryn, Kayla N.; Yoskowitz, Nicole A.; Cimino, James J.; Patel, Vimla L.

2009-01-01

Despite public health initiatives targeting rapid action in response to symptoms of myocardial infarction (MI), people continue to delay in going to a hospital when experiencing these symptoms due to lack of recognition as cardiac-related. The objective of this research was to characterize lay individuals' knowledge of symptoms of acute myocardial…

Rescue pulmonary vein isolation for hemodynamically unstable atrial fibrillation storm in a patient with an acute extensive myocardial infarction.

PubMed

Morishima, Itsuro; Sone, Takahito; Tsuboi, Hideyuki; Mukawa, Hiroaki

2012-11-26

New-onset atrial fibrillation in patients hospitalized for an acute myocardial infarction often leads to hemodynamic deterioration and has serious adverse prognostic implications; mortality is particularly high in patients with congestive heart failure and/or a reduced left ventricular ejection fraction. The mechanism of atrial fibrillation in the context of an acute myocardial infarction has not been well characterized and an effective treatment other than optimal medical therapy and mechanical hemodynamic support are expected. A 71 year-old male with an acute myocardial infarction due to an occlusion of the left main coronary artery was treated with percutaneous coronary intervention. He had developed severe congestive heart failure with a left ventricular ejection fraction of 34%. The systemic circulation was maintained with an intraaortic balloon pump, continuous hemodiafiltration, and mechanical ventilation until atrial fibrillation occurred on day 3 which immediately led to cardiogenic shock. Because atrial fibrillation was refractory to intravenous amiodarone, beta-blockers, and a total of 15 electrical cardioversions, the patient underwent emergent radiofrequency catheter ablation on day 4. Soon after electrical cardioversion, ectopies from the right superior pulmonary vein triggered the initiation of atrial fibrillation. The right pulmonary veins were isolated during atrial fibrillation. Again, atrial fibrillation was electrically cardioverted, then, sinus rhythm was restored. Subsequently, the left pulmonary veins were isolated. The stabilization of the hemodynamics was successfully achieved with an increase in the blood pressure and urine volume. Hemodiafiltration and amiodarone were discontinued. The patient had been free from atrial fibrillation recurrence until he suddenly died due to ventricular fibrillation on day 9. To the best of our knowledge, this is the first report of pulmonary vein isolation for a rescue purpose applied in a patient with

The History of Primary Angioplasty and Stenting for Acute Myocardial Infarction.

PubMed

Smilowitz, Nathaniel R; Feit, Frederick

2016-01-01

The evolution of the management of acute myocardial infarction (MI) has been one of the crowning achievements of modern medicine. At the turn of the twentieth century, MI was an often-fatal condition. Prolonged bed rest served as the principal treatment modality. Over the past century, insights into the pathophysiology of MI revolutionized approaches to management, with the sequential use of surgical coronary artery revascularization, thrombolytic therapy, and percutaneous coronary intervention (PCI) with primary coronary angioplasty, and placement of intracoronary stents. The benefits of prompt revascularization inspired systems of care to provide rapid access to PCI. This review provides a historical context for our current approach to primary PCI for acute MI.

Serum Acylcarnitines and Risk of Cardiovascular Death and Acute Myocardial Infarction in Patients With Stable Angina Pectoris.

PubMed

Strand, Elin; Pedersen, Eva R; Svingen, Gard F T; Olsen, Thomas; Bjørndal, Bodil; Karlsson, Therese; Dierkes, Jutta; Njølstad, Pål R; Mellgren, Gunnar; Tell, Grethe S; Berge, Rolf K; Svardal, Asbjørn; Nygård, Ottar

2017-02-03

Excess levels of serum acylcarnitines, which are intermediate products in metabolism, have been observed in metabolic diseases such as type 2 diabetes mellitus. However, it is not known whether acylcarnitines may prospectively predict risk of cardiovascular death or acute myocardial infarction in patients with stable angina pectoris. This study included 4164 patients (median age, 62 years; 72% men). Baseline serum acetyl-, octanoyl-, palmitoyl-, propionyl-, and (iso)valerylcarnitine were measured using liquid chromatography/tandem mass spectrometry. Hazard ratios (HRs) and 95% CIs for quartile 4 versus quartile 1 are reported. The multivariable model included age, sex, body mass index, fasting status, current smoking, diabetes mellitus, apolipoprotein A1, apolipoprotein B, creatinine, left ventricular ejection fraction, extent of coronary artery disease, study center, and intervention with folic acid or vitamin B6. During median 10.2 years of follow-up, 10.0% of the patients died of cardiovascular disease and 12.8% suffered a fatal or nonfatal acute myocardial infarction. Higher levels of the even-chained acetyl-, octanoyl-, and palmitoyl-carnitines were significantly associated with elevated risk of cardiovascular death, also after multivariable adjustments (HR [95% CI]: 1.52 [1.12, 2.06]; P=0.007; 1.73 [1.23, 2.44]; P=0.002; and 1.61 [1.18, 2.21]; P=0.003, respectively), whereas their associations with acute myocardial infarction were less consistent. Among patients with suspected stable angina pectoris, elevated serum even-chained acylcarnitines were associated with increased risk of cardiovascular death and, to a lesser degree with acute myocardial infarction, independent of traditional risk factors. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00354081. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

Perioperative Assessment of Myocardial Deformation

PubMed Central

Duncan, Andra E.; Alfirevic, Andrej; Sessler, Daniel I.; Popovic, Zoran B.; Thomas, James D.

2014-01-01

assess components of myocardial systolic and diastolic function. Myocardial deformation analysis is based on either Doppler or a non-Doppler technique, called speckle-tracking echocardiography. Myocardial deformation analysis provides quantitative measures of global and regional myocardial function for use in the perioperative care of the surgical patient. For example, coronary graft occlusion after coronary artery bypass grafting is detected by an acute reduction in strain in the affected coronary artery territory. In addition, assessment of left ventricular mechanics detects underlying myocardial pathology before abnormalities become apparent on conventional echocardiography. Certainly, patients with aortic regurgitation demonstrate reduced longitudinal strain before reduction in LVEF occurs, which allows detection of subclinical left ventricular dysfunction and predicts increased risk for heart failure and impaired myocardial function after surgical repair. In this review we describe the principles, techniques, and clinical application of myocardial deformation analysis. PMID:24557101

Pyridostigmine prevents peripheral vascular endothelial dysfunction in rats with myocardial infarction.

PubMed

Qin, Fangfang; Lu, Yi; He, Xi; Zhao, Ming; Bi, Xueyuan; Yu, Xiaojiang; Liu, Jinjun; Zang, Weijin

2014-03-01

1. Myocardial infarction (MI) is characterized by the withdrawal of vagal activity and increased sympathetic activity. We have shown previously that pyridostigmine (PYR), an acetylcholinesterase inhibitor, was able to improve vagal activity and ameliorate cardiac dysfunction following MI. However, the effect of PYR on endothelial dysfunction in peripheral arteries after MI remains unclear. 2. In the present study, MI was induced by coronary artery ligation in adult Sprague-Dawley rats. Rats were treated intragastrically with saline or PYR (approximately 31 mg/kg per day) for 2 weeks, at which time haemodynamic and parasympathetic parameters and the vascular reactivity of isolated mesenteric arteries were measured and the ultrastructure of the endothelium evaluated. 3. Compared with the MI group, PYR not only improved cardiac function, vagal nerve activity and endothelial impairment, but also reduced intravascular superoxide anion and malondialdehyde. In addition, in the PYR-treated MI group, nitric oxide (NO) bioavailability was increased and attenuated endothelium-dependent relaxations were improved, whereas restored vasodilator responses were inhibited by N(G)-nitro-L-arginine methyl ester. 4. Based on our results, PYR is able to attenuate the impairment of peripheral endothelial function and maintain endothelial ultrastructural integrity in MI rats by inhibiting reactive oxygen species production, enhancing NO bioavailability and improving vagal activity. © 2014 Wiley Publishing Asia Pty Ltd.

Radiologic evaluation of acute chest pain--suspected myocardial ischemia.

PubMed

Stanford, William

2007-08-15

The American College of Radiology has developed appropriateness criteria for a number of clinical conditions and procedures. Criteria are available on imaging tests used in the evaluation of acute chest pain--suspected myocardial ischemia. Imaging tests for a suspected cardiac etiology include transthoracic echocardiography, transesophageal echocardiography, radionuclide perfusion imaging, radionuclide ventriculography, radionuclide infarct avid imaging, and positron emission tomography. If the cardiac ischemic work-up is negative or indeterminate, applicable tests include chest radiography; conventional, multidetector, and electron beam computed tomography; and magnetic resonance imaging. A summary of the criteria, with the advantages and limitations of each test, is presented in this article.

Assessment of subclinical right ventricular systolic dysfunction in coal miners using myocardial isovolumic acceleration.

PubMed

Ozcan Abacıoglu, Ozge; Kaplan, Mehmet; Abacıoglu, Serkan; Quisi, Ala

2017-09-01

Several studies have been conducted regarding the effects of coal mining on the respiratory system. However, there is a lack of data concerning potential effects of coal mining on the cardiovascular system. In this study, we aimed to evaluate the potential subclinical right and left ventricular dysfunction in coal miners. This single-center, prospective study included a total of 102 patients. Patient and control groups consisted of 54 coal miners and 48 healthy men, respectively. All patients underwent 12-lead electrocardiography, transthoracic echocardiography, and pulmonary function test. As compared to control group, coal miners had significantly higher right ventricular myocardial performance index (RVMPI) (0.41 ± 0.03 vs 0.37 ± 0.02, P < .001), lower right ventricular fractional area change (RVFAC) (33.55% ± 6.70% vs 37.04 ± 9.26 P < .05), lower tricuspid annular plane systolic excursion (TAPSE) (1.54 ± 0.17 vs 1.73 ± 0.25, P < .001), lower myocardial isovolumic acceleration (IVA) (2.13 ± 0.16 vs 2.56 ± 0.36 P < .001) and decreased aortic distensibility (AD) (4.14 ± 2.18 vs 6.63 ± 3.91 P < .001). All of the echocardiographic parameters were positively correlated with exposure time to coal mine dust, except IVA. Echocardiographic parameters of both right and left ventricular dysfunction, including RVMPI, RVFAC, TAPSE, IVA, and AD, are impaired in coal miners. © 2017 The Authors Echocardiography Published by Wiley Periodicals, Inc.

[The Brazilian Hospital Information System and the acute myocardial infarction hospital care].

PubMed

Escosteguy, Claudia Caminha; Portela, Margareth Crisóstomo; Medronho, Roberto de Andrade; de Vasconcellos, Maurício Teixeira Leite

2002-08-01

To analyze the applicability of the Brazilian Unified Health System's national hospital database to evaluate the quality of acute myocardial infarction hospital care. It was evaluated 1,936 hospital admission forms having acute myocardial infarction (AMI) as primary diagnosis in the municipal district of Rio de Janeiro, Brazil, in 1997. Data was collected from the national hospital database. A stratified random sampling of 391 medical records was also evaluated. AMI diagnosis agreement followed the literature criteria. Variable accuracy analysis was performed using kappa index agreement. The quality of AMI diagnosis registered in hospital admission forms was satisfactory according to the gold standard of the literature. In general, the accuracy of the variables demographics (sex, age group), process (medical procedures and interventions), and outcome (hospital death) was satisfactory. The accuracy of demographics and outcome variables was higher than the one of process variables. Under registration of secondary diagnosis was high in the forms and it was the main limiting factor. Given the study findings and the widespread availability of the national hospital database, it is pertinent its use as an instrument in the evaluation of the quality of AMI medical care.

Remote ischaemic postconditioning protects the heart during acute myocardial infarction in pigs

PubMed Central

Andreka, Gyorgy; Vertesaljai, Marton; Szantho, Gergely; Font, Gusztav; Piroth, Zsolt; Fontos, Geza; Juhasz, Eszter D; Szekely, Laszlo; Szelid, Zsolt; Turner, Mark S; Ashrafian, Houman; Frenneaux, Michael P

2007-01-01

Background Ischaemic preconditioning results in a reduction in ischaemic‐reperfusion injury to the heart. This beneficial effect is seen both with direct local preconditioning of the myocardium and with remote preconditioning of easily accessible distant non‐vital limb tissue. Ischaemic postconditioning with a comparable sequence of brief periods of local ischaemia, when applied immediately after the ischaemic insult, confers benefits similar to preconditioning. Objective To test the hypothesis that limb ischaemia induces remote postconditioning and hence reduces experimental myocardial infarct size in a validated swine model of acute myocardial infarction. Methods Acute myocardial infarction was induced in 24 pigs with 90 min balloon inflations of the left anterior descending coronary artery. Remote ischaemic postconditioning was induced in 12 of the pigs by four 5 min cycles of blood pressure cuff inflation applied to the lower limb immediately after the balloon deflation. Infarct size was assessed by measuring 72 h creatinine kinase release, MRI scan and immunohistochemical analysis. Results Area under the curve of creatinine kinase release was significantly reduced in the postconditioning group compared with the control group with a 26% reduction in the infarct size (p<0.05). This was confirmed by MRI scanning and immunohistochemical analysis that revealed a 22% (p<0.05) and a 47.52% (p<0.01) relative reduction in the infarct size, respectively. Conclusion Remote ischaemic postconditioning is a simple technique to reduce infarct size without the hazards and logistics of multiple coronary artery balloon inflations. This type of conditioning promises clear clinical potential. PMID:17449499

Safety of air travel following acute myocardial infarction.

PubMed

Roby, Howard; Lee, Anna; Hopkins, Andrew

2002-02-01

initiated in one patient with chest pain that turned out to be non-ischemic when the Holter traces were later analyzed. This study suggests that, provided that care is taken during the immediate preflight and postflight phases not to overexert the patients, neither supplemental oxygen nor medical escorts are needed in the transportation of patients who fly 2 wk after acute myocardial infarction.

G-CSF in acute myocardial infarction - experimental and clinical findings.

PubMed

Ince, Hüseyin; Petzsch, Michael; Rehders, Tim C; Dunkelmann, Simone; Nienaber, Christoph A

2006-09-01

Early data from clinical studies suggest that intracoronary injection of autologous progenitor cells may beneficially affect postinfarction remodeling and perfusion. Beyond intracoronary infusion of autologous bone marrow mononuclear CD34+ cells (MNCCD34+), mobilization of stem cells by G-CSF has recently attracted attention because of various advantages such as the noninvasive nature of MNCCD34+ mobilization by subcutaneous injections. It is the aim of the present work to give an overview about the current experimental and clinical findings of G-CSF treatment in acute myocardial infarction.

Outcomes with invasive vs conservative management of cardiogenic shock complicating acute myocardial infarction.

PubMed

Bangalore, Sripal; Gupta, Navdeep; Guo, Yu; Lala, Anuradha; Balsam, Leora; Roswell, Robert O; Reyentovich, Alex; Hochman, Judith S

2015-06-01

In the SHOCK trial, an invasive strategy of early revascularization was associated with a significant mortality benefit at 6 months when compared with initial stabilization in patients with cardiogenic shock complicating acute myocardial infarction. Our objectives were to evaluate the data on real-world practice and outcomes of invasive vs conservative management in patients with cardiogenic shock. We analyzed data from the Nationwide Inpatient Sample from 2002 to 2011 with primary discharge diagnosis of acute myocardial infarction and secondary diagnosis of cardiogenic shock. Propensity score matching was used to assemble a cohort of patients managed invasively (with cardiac catheterization, percutaneous coronary intervention, or coronary artery bypass graft surgery) vs conservatively with similar baseline characteristics. The primary outcome was in-hospital mortality. We identified 60,833 patients with cardiogenic shock, of which 20,644 patients (10,322 in each group) with similar propensity scores, including 11,004 elderly patients (≥75 years), were in the final analysis. Patients who underwent invasive management had 59% lower odds of in-hospital mortality (37.7% vs 59.7%; odds ratio [OR] 0.41; 95% confidence interval [CI], 0.39-0.43; P < .0001) when compared with those managed conservatively. This lower mortality was consistently seen across all tested subgroups; specifically in the elderly (≥75 years) (44.0% vs 63.6%; OR 0.45; 95% CI, 0.42-0.49; P < .0001) and those younger than 75 years (30.6% vs 55.1%; OR 0.36; 95% CI, 0.33-0.39; P < .0001), although the magnitude of risk reduction differed (Pinteraction < .0001). In this largest cohort of patients with cardiogenic shock complicating acute myocardial infarction, patients managed invasively had significantly lower mortality when compared with those managed conservatively, even in the elderly. Our results emphasize the need for aggressive management in this high-risk subgroup. Copyright © 2015 Elsevier

Non-arrhythmic therapy of ventricular tachyarrhythmias and sudden cardiac death after acute myocardial infarction.

PubMed

Schweitzer, P

2006-12-01

The management of ventricular tachyarrhythmias and prevention of sudden cardiac death after acute myocardial infarction (AMI) underwent important evolution. In the CAST study, encanaide and other antiarrhythmic drugs were not only ineffective but also increased mortality after myocardial infarction. Amiodarone had some beneficial effect on arrhythmic events without improving survival, and ICDs failed to improve outcome early after AMI. In comparison, short and long term survival benefits of beta blockers, angiotensine converting enzyme inhibitors and aldosterone antagonists after AMI is well established. This review discusses the role of non-arrhythmic therapy in the prevention of ventricular tachyarrhythmia's and sudden cardiac death after AMI.

It's a trap! Clinical similarities and subtle ECG differences between takotsubo cardiomyopathy and myocardial infarction.

PubMed

Vivo, Rey P; Krim, Selim R; Hodgson, John

2008-11-01

We describe a 65-year-old woman with a history of hypertension and smoking who presented with an acute episode of chest pain precipitated by severe emotional stress. Her initial electrocardiogram done in the emergency room showed non-specific T wave changes in the lateral leads and her cardiac troponin levels were mildly elevated. Because of her clinical presentation, she was admitted with a presumptive diagnosis of acute myocardial infarction and managed with antiplatelet and anticoagulant therapy. Coronary angiogram did not reveal coronary artery disease and left ventriculography showed findings consistent with apical ballooning syndrome or takotsubo cardiomyopathy. Subsequent electrocardiograms displayed dramatic changes including T wave inversions, QT interval prolongation and U waves. The patient remained asymptomatic and recovered uneventfully. Three weeks post-discharge, an echocardiogram documented resolved left ventricular dysfunction. We describe the clinical features and highlight the electrocardiographic findings that may help differentiate takotsubo cardiomyopathy from myocardial infarction.

ST-Segment Elevation Myocardial Infarction with Acute Stent Thrombosis Presenting as Intractable Hiccups: An Unusual Case

PubMed Central

Zhang, Fan; Tongo, Nosakhare Douglas; Hastings, Victoria; Kanzali, Parisa; Zhu, Ziqiang; Chadow, Hal; Rafii, Shahrokh E.

2017-01-01

Patient: Male, 51 Final Diagnosis: ST-segment elevation myocardial infarction with acute stent thrombosis Symptoms: Chest pain • hiccups Medication: — Clinical Procedure: — Specialty: Cardiology Objective: Unusual clinical course Background: Acute coronary syndrome (ACS) can present with atypical chest pain or symptoms not attributed to heart disease, such as indigestion. Hiccups, a benign and self-limited condition, can become persistent or intractable with overlooked underlying etiology. There are various causes of protracted hiccups, including metabolic abnormalities, psychogenic disorders, malignancy, central nervous system pathology, medications, pulmonary disorders, or gastrointestinal etiologies. It is rarely attributed to cardiac disease. Case Report: We report a case of intractable hiccups in a 51-year-old male with cocaine related myocardial infarction (MI) before and after stent placement. Coronary angiogram showed in-stent thrombosis of the initial intervention. Following thrombectomy, balloon angioplasty, and stent, the patient recovered well without additional episodes of hiccups. Although hiccups are not known to present with a predilection for a particular cause of myocardial ischemia, this case may additionally be explained by the sympathomimetic effects of cocaine, which lead to vasoconstriction of coronary arteries. Conclusions: Hiccups associated with cardiac enzyme elevation and EKG ST-segment elevation before and after percutaneous coronary intervention (PCI) maybe a manifestation of acute MI with or without stent. The fact that this patient was a cocaine user may have contributed to the unique presentation. PMID:28455489

Educational attainment and differences in relative survival after acute myocardial infarction in Norway: a registry-based population study.

PubMed

Klitkou, Søren Toksvig; Wangen, Knut R

2017-08-28

Although there is a broad societal interest in socioeconomic differences in survival after an acute myocardial infarction, only a few studies have investigated how such differences relate to the survival in general population groups. We aimed to investigate education-specific survival after acute myocardial infarction and to compare this with the survival of corresponding groups in the general population. Our study included the entire population of Norwegian patients admitted to hospitals for acute myocardial infarction during 2008-2010, with a 6- year follow-up period. Patient survival was measured relative to the expected survival in the general population for three educational groups: primary, secondary and tertiary. Education, sex, age and calendar year-specific expected survival were obtained from population life tables and adjusted for the presence of infarction-related mortality. Six-year patient survivals were 56.3% (55.3-57.2) and 65.5% (65.6-69.3) for the primary and tertiary educational groups (95% CIs), respectively. Also 6-year relative survival was markedly lower for the primary educational group: 70.2% (68.6-71.8) versus 81.2% (77.4-84.4). Throughout the follow-up period, patient survival tended to remain lower than the survival in the general population with the same educational background. Both patient survival and relative survival after acute myocardial infarction are positively associated with educational level. Our findings may suggest that secondary prevention has been more effective for the highly educated. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Results of the Croatian Primary Percutaneous Coronary Intervention Network for patients with ST-segment elevation acute myocardial infarction.

PubMed

Nikolić Heitzler, Vjeran; Babic, Zdravko; Milicic, Davor; Bergovec, Mijo; Raguz, Miroslav; Mirat, Jure; Strozzi, Maja; Plazonic, Zeljko; Giunio, Lovel; Steiner, Robert; Starcevic, Boris; Vukovic, Ivica

2010-05-01

The Republic of Croatia, with a gross domestic product per capita of US$11,554 in 2008, is an economically less-developed Western country. The goal of the present investigation was to prove that a well-organized primary percutaneous coronary intervention network in an economically less-developed country equalizes the prospects of all patients with acute ST-segment elevation myocardial infarction at a level comparable to that of more economically developed countries. We prospectively investigated 1,190 patients with acute ST-segment elevation myocardial infarction treated with primary PCI in 8 centers across Croatia (677 nontransferred and 513 transferred). The postprocedural Thrombolysis In Myocardial Infarction flow, in-hospital mortality, and incidence of major adverse cardiovascular events (ie, mortality, pectoral angina, restenosis, reinfarction, coronary artery bypass graft, and cerebrovascular accident rate) during 6 months of follow-up were compared between the nontransferred and transferred subgroups and in the subgroups of older patients, women, and those with cardiogenic shock. In all investigated patients, the average door-to-balloon time was 108 minutes, and the total ischemic time was 265 minutes. Postprocedural Thrombolysis In Myocardial Infarction 3 flow was established in 87.1% of the patients, and the in-hospital mortality rate was 4.4%. No statistically significant difference was found in the results of treatment between the transferred and nontransferred patients overall or in the subgroups of patients >75 years, women, and those with cardiogenic shock. In conclusion, the Croatian Primary Percutaneous Coronary Intervention Network has ensured treatment results of acute ST-segment elevation myocardial infarction comparable to those of randomized studies and registries of more economically developed countries. Copyright 2010 Elsevier Inc. All rights reserved.

Experimental myocardial infarction

PubMed Central

Kumar, Raj; Joison, Julio; Gilmour, David P.; Molokhia, Farouk A.; Pegg, C. A. S.; Hood, William B.

1971-01-01

The hemodynamic effects of tachycardia induced by atrial pacing were investigated in left ventricular failure of acute and healing experimental myocardial infarction in 20 intact, conscious dogs. Myocardial infarction was produced by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 10-15 days prior to the study. 1 hr after acute myocardial infarction, atrial pacing at a rate of 180 beats/min decreased left ventricular end-diastolic pressure from 19 to 8 mm Hg and left atrial pressure from 17 to 12 mm Hg, without change in cardiac output. In the healing phase of myocardial infarction 1 wk later, atrial pacing decreased left ventricular end-diastolic pressure from 17 to 9 mm Hg and increased the cardiac output by 37%. This was accompanied by evidence of peripheral vasodilation. In two dogs with healing anterior wall myocardial infarction, left ventricular failure was enhanced by partial occlusion of the circumflex coronary artery. Both the dogs developed pulmonary edema. Pacing improved left ventricular performance and relieved pulmonary edema in both animals. In six animals propranolol was given after acute infarction, and left ventricular function deteriorated further. However the pacing-induced augmentation of cardiac function was unaltered and, hence, is not mediated by sympathetics. The results show that the spontaneous heart rate in left ventricular failure of experimental canine myocardial infarction may be less than optimal and that maximal cardiac function may be achieved at higher heart rates. Images PMID:4395910

National trends in rates of death and hospital admissions related to acute myocardial infarction, heart failure and stroke, 1994–2004

PubMed Central

Tu, Jack V.; Nardi, Lorelei; Fang, Jiming; Liu, Juan; Khalid, Laila; Johansen, Helen

2009-01-01

Background Rates of death from cardiovascular and cerebrovascular diseases have been steadily declining over the past few decades. Whether such declines are occurring to a similar degree for common disorders such as acute myocardial infarction, heart failure and stroke is uncertain. We examined recent national trends in mortality and rates of hospital admission for these 3 conditions. Methods We analyzed mortality data from Statistic Canada’s Canadian Mortality Database and data on hospital admissions from the Canadian Institute for Health Information’s Hospital Morbidity Database for the period 1994–2004. We determined age- and sex-standardized rates of death and hospital admissions per 100 000 population aged 20 years and over as well as in-hospital case-fatality rates. Results The overall age- and sex-standardized rate of death from cardiovascular disease in Canada declined 30.0%, from 360.6 per 100 000 in 1994 to 252.5 per 100 000 in 2004. During the same period, the rate fell 38.1% for acute myocardial infarction, 23.5% for heart failure and 28.2% for stroke, with improvements observed across most age and sex groups. The age- and sex-standardized rate of hospital admissions decreased 27.6% for stroke and 27.2% for heart failure. The rate for acute myocardial infarction fell only 9.2%. In contrast, the relative decline in the inhospital case-fatality rate was greatest for acute myocardial infarction (33.1%; p < 0.001). Much smaller relative improvements in case-fatality rates were noted for heart failure (8.1%) and stroke (8.9%). Interpretation The rates of death and hospital admissions for acute myocardial infarction, heart failure and stroke in Canada changed at different rates over the 10-year study period. Awareness of these trends may guide future efforts for health promotion and health care planning and help to determine priorities for research and treatment. PMID:19546444

Evaluation of the NICE mini-GRACE risk scores for acute myocardial infarction using the Myocardial Ischaemia National Audit Project (MINAP) 2003-2009: National Institute for Cardiovascular Outcomes Research (NICOR).

PubMed

Simms, Alexander D; Reynolds, Stephanie; Pieper, Karen; Baxter, Paul D; Cattle, Brian A; Batin, Phillip D; Wilson, John I; Deanfield, John E; West, Robert M; Fox, Keith A A; Hall, Alistair S; Gale, Christopher P

2013-01-01

To evaluate the performance of the National Institute for Health and Clinical Excellence (NICE) mini-Global Registry of Acute Coronary Events (GRACE) (MG) and adjusted mini-GRACE (AMG) risk scores. Retrospective observational study. 215 acute hospitals in England and Wales. 137 084 patients discharged from hospital with a diagnosis of acute myocardial infarction (AMI) between 2003 and 2009, as recorded in the Myocardial Ischaemia National Audit Project (MINAP). Model performance indices of calibration accuracy, discriminative and explanatory performance, including net reclassification index (NRI) and integrated discrimination improvement. Of 495 263 index patients hospitalised with AMI, there were 53 196 ST elevation myocardial infarction and 83 888 non-ST elevation myocardial infarction (NSTEMI) (27.7%) cases with complete data for all AMG variables. For AMI, AMG calibration was better than MG calibration (Hosmer-Lemeshow goodness of fit test: p=0.33 vs p<0.05). MG and AMG predictive accuracy and discriminative ability were good (Brier score: 0.10 vs 0.09; C statistic: 0.82 and 0.84, respectively). The NRI of AMG over MG was 8.1% (p<0.05). Model performance was reduced in patients with NSTEMI, chronic heart failure, chronic renal failure and in patients aged ≥85 years. The AMG and MG risk scores, utilised by NICE, demonstrated good performance across a range of indices using MINAP data, but performed less well in higher risk subgroups. Although indices were better for AMG, its application may be constrained by missing predictors.

Lessons from the management of acute myocardial infarction.

PubMed

Pearson, M

2005-05-01

The National Service Framework for coronary heart disease set a number of challenging targets for the care of patients following an acute myocardial infarction. The Myocardial Infarction National Audit Project (MINAP) was devised to monitor progress and has been notably successful in winning professional support and participation and helping trusts to meet these targets. The new challenge is in translating this success to other areas of medicine. Heart failure is one such area, although it poses a number of difficulties relating primarily to disease definition and the definition of a successful outcome. MINAP was overseen by a multidisciplinary group of stakeholders, including patient organisations, and was project managed by a professionally led team at the Royal College of Physicians. Successful projects must retain confidence of all stakeholders and in part this depends on ensuring that timelines are met. Central monitoring of returns and anticipation of problems has been an important component of data completeness and quality. Next day updates to those collecting the data and more detailed quarterly reports for clinicians and chief executives within days of quarter end have been vital. Change depends on clinicians and managers working together. But most importantly, the attention to detail outlined above means the data have been believed and the resulting change for patients has been remarkable.

Changing paradigms in thrombolysis in acute myocardial infarction.

PubMed

Gotsman, M S; Rozenman, Y; Admon, D; Mosseri, M; Lotan, C; Zahger, D; Weiss, A T

1997-05-23

Acute myocardial infarction occurs when a ruptured coronary artery plaque causes sudden thrombotic occlusion of a coronary artery and cessation of coronary artery blood flow. This paper reviews the underlying coronary pathology in progressive coronary atherosclerosis, mechanisms of plaque rupture and arterial occlusion and the time relationship between coronary occlusion and myocardial necrosis. Reperfusion can be achieved by chemical thrombolysis with different thrombolytic agents. Early lysis is achieved best by prehospital administration, a transtelephonic monitor, a mobile intensive care unit, active general practitioner treatment or by warning the emergency room of impending arrival of a patient. Thrombolytic therapy may be unsuccessful and not achieve Grade III TIMI flow in less than 4 h (or even 2 h) due to inadequate or intermittent perfusion or reocclusion. Adjuvant therapy includes aspirin and platelet receptor antagonists. Bleeding is a constant danger. Direct percutaneous transluminal coronary angioplasty (PTCA) may be as effective or better than chemical thrombolysis. Reperfusion protects the myocardium and salvages viable tissue. It also improves mechanical remodelling of the ventricle. Long-term follow-up has shown that quantum leaps of fresh coronary occlusion causes step-wise progression in patient disability and that further early, prompt reperfusion can salvage myocardium and prevent this inexorable progress of the disease.

Diagnostics on acute myocardial infarction: Cardiac troponin biomarkers.

PubMed

Fathil, M F M; Md Arshad, M K; Gopinath, Subash C B; Hashim, U; Adzhri, R; Ayub, R M; Ruslinda, A R; Nuzaihan M N, M; Azman, A H; Zaki, M; Tang, Thean-Hock

2015-08-15

Acute myocardial infarction or myocardial infarction (MI) is a major health problem, due to diminished flow of blood to the heart, leads to higher rates of mortality and morbidity. Data from World Health Organization (WHO) accounted 30% of global death annually and expected more than 23 million die annually by 2030. This fatal effects trigger the need of appropriate biomarkers for early diagnosis, thus countermeasure can be taken. At the moment, the most specific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac troponin T (cTnT) which have been considered as 'gold standard'. Due to higher specificity, determination of the level of cardiac troponins became a predominant indicator for MI. Several ways of diagnostics have been formulated, which include enzyme-linked immunosorbent assay, chemiluminescent, fluoro-immunoassays, electrical detections, surface plasmon resonance, and colorimetric protein assay. This review represents and elucidates the strategies, methods and detection levels involved in these diagnostics on cardiac superior biomarkers. The advancement, sensitivity, and limitations of each method are also discussed. In addition, it concludes with a discussion on the point-of care (POC) assay for a fast, accurate and ability of handling small sample measurement of cardiac biomarker. Copyright © 2015 Elsevier B.V. All rights reserved.

Protective effects of combination of quercetin and α-tocopherol on mitochondrial dysfunction and myocardial infarct size in isoproterenol-treated myocardial infarcted rats: biochemical, transmission electron microscopic, and macroscopic enzyme mapping evidences.

PubMed

Punithavathi, V R; Stanely Mainzen Prince, P

2010-01-01

Mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. We evaluated the combined protective effects of quercetin and α-tocopherol on mitochondrial damage and myocardial infarct size in isoproterenol-induced myocardia- infarcted rats. Rats were pretreated with quercetin (10 mg/kg) alone, α-tocopherol (10 mg/kg) alone, and combination of quercetin (10 mg/kg) and α-tocopherol (10 mg/kg) orally using an intragastric tube daily for 14 days. After pretreatment, rats were induced myocardial infarction by isoproterenol (100 mg/kg) at an interval of 24 h for 2 days. Isoproterenol treatment caused significant increase in mitochondrial lipid peroxides with significant decrease in mitochondrial antioxidants. Significant decrease in the activities of isocitrate, succinate, malate, and α-ketoglutarate and NADH dehydrogenases and cytochrome-c-oxidase, significant increase in calcium, and significant decrease in adenosine triphosphate were observed in mitochondria of myocardial infarcted rats. Combined pretreatment with quercetin and α-tocopherol normalized all the biochemical parameters and preserved the integrity of heart tissue and restored normal mitochondrial function in myocardial-infarcted rats. Transmission electron microscopic findings on heart mitochondria and macroscopic enzyme mapping assay on the size of myocardial infarct also correlated with these biochemical parameters. The present study showed that combined pretreatment was highly effective than single pretreatment. Copyright 2010 Wiley Periodicals, Inc.

Permanent stress may be the trigger of an acute myocardial infarction on the first work-day of the week.

PubMed

Bodis, Jozsef; Boncz, Imre; Kriszbacher, Ildiko

2010-10-29

Numerous studies have reported the weekly variation of an acute myocardial infarction. The Monday peek has been connected with higher rate of physical and mental, work-related stress. We wished to study the weekly variation of an acute myocardial infarction (AMI) in the group of workers and pensioners, and to find out whether National Holidays on the first day of the week could influence the weekly rhythm of an acute myocardial infarction. We carried out the retrospective analysis of patients admitted to Hungarian hospitals with the diagnose of an AMI (n=90,187) between 2002 and 2007. According to the morbidity data of an AMI, the weekly peek was detected on the first work-day of the week, showing a gradually decreasing tendency until the end of the week. Morbidity rates on Mondays being National Holidays were similar to the number of events on Saturdays and Sundays (Z=-24,431; p<0.001). There was a significant difference between the number of events on work-days and weekends (Z=-27,321; p<0.001). No marked difference was found between workers under the age of 65 and pensioners above the age of 65, or between the two sexes. The results of our study reveal that the occurrence of an AMI shows characteristic changes throughout the days of the week, and the first work-days of the week may be related to higher incidence of an acute myocardial infarction. Crown Copyright © 2009. Published by Elsevier Ireland Ltd. All rights reserved.

Quality of Care for Acute Myocardial Infarction in Rural and Urban US Hospitals

ERIC Educational Resources Information Center

Baldwin, Laura-Mae; MacLehose, Richard F.; Hart, L. Gary; Beaver, Shelli K.; Every,Nathan; Chan,Leighton

2004-01-01

Context: Acute myocardial infarction (AMI) is a common and important cause of admission to US rural hospitals, as transport of patients with AMI to urban settings can result in unacceptable delays in care. Purpose: To examine the quality of care for patients with AMI in rural hospitals with differing degrees of remoteness from urban centers.…

PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock.

PubMed

Thiele, Holger; Akin, Ibrahim; Sandri, Marcus; Fuernau, Georg; de Waha, Suzanne; Meyer-Saraei, Roza; Nordbeck, Peter; Geisler, Tobias; Landmesser, Ulf; Skurk, Carsten; Fach, Andreas; Lapp, Harald; Piek, Jan J; Noc, Marko; Goslar, Tomaž; Felix, Stephan B; Maier, Lars S; Stepinska, Janina; Oldroyd, Keith; Serpytis, Pranas; Montalescot, Gilles; Barthelemy, Olivier; Huber, Kurt; Windecker, Stephan; Savonitto, Stefano; Torremante, Patrizia; Vrints, Christiaan; Schneider, Steffen; Desch, Steffen; Zeymer, Uwe

2017-12-21

In patients who have acute myocardial infarction with cardiogenic shock, early revascularization of the culprit artery by means of percutaneous coronary intervention (PCI) improves outcomes. However, the majority of patients with cardiogenic shock have multivessel disease, and whether PCI should be performed immediately for stenoses in nonculprit arteries is controversial. In this multicenter trial, we randomly assigned 706 patients who had multivessel disease, acute myocardial infarction, and cardiogenic shock to one of two initial revascularization strategies: either PCI of the culprit lesion only, with the option of staged revascularization of nonculprit lesions, or immediate multivessel PCI. The primary end point was a composite of death or severe renal failure leading to renal-replacement therapy within 30 days after randomization. Safety end points included bleeding and stroke. At 30 days, the composite primary end point of death or renal-replacement therapy had occurred in 158 of the 344 patients (45.9%) in the culprit-lesion-only PCI group and in 189 of the 341 patients (55.4%) in the multivessel PCI group (relative risk, 0.83; 95% confidence interval [CI], 0.71 to 0.96; P=0.01). The relative risk of death in the culprit-lesion-only PCI group as compared with the multivessel PCI group was 0.84 (95% CI, 0.72 to 0.98; P=0.03), and the relative risk of renal-replacement therapy was 0.71 (95% CI, 0.49 to 1.03; P=0.07). The time to hemodynamic stabilization, the risk of catecholamine therapy and the duration of such therapy, the levels of troponin T and creatine kinase, and the rates of bleeding and stroke did not differ significantly between the two groups. Among patients who had multivessel coronary artery disease and acute myocardial infarction with cardiogenic shock, the 30-day risk of a composite of death or severe renal failure leading to renal-replacement therapy was lower among those who initially underwent PCI of the culprit lesion only than among those

Comparison of gender-specific mortality in patients < 70 years versus ≥ 70 years old with acute myocardial infarction.

PubMed

Ishihara, Masaharu; Inoue, Ichiro; Kawagoe, Takuji; Shimatani, Yuji; Miura, Fumiharu; Nakama, Yasuharu; Dai, Kazuoki; Ootani, Takayuki; Ooi, Kuniomi; Ikenaga, Hiroki; Miki, Takashi; Nakamura, Masayuki; Kishimoto, Shinji; Sumimoto, Youji

2011-09-15

The aim of the present study was to investigate the gender-specific mortality after acute myocardial infarction in those aged < 70 years versus ≥ 70 years. The present study consisted of 2,677 consecutive patients with acute myocardial infarction who had undergone coronary angiography within 24 hours after the onset of symptoms. The patients were divided into 2 groups: 1,810 patients < 70 years old and 867 patients ≥ 70 years old. Women were older and had a greater incidence of hypertension and diabetes mellitus and a lower incidence of current smoking and previous myocardial infarction in both groups. The in-hospital mortality rate was significantly greater in women ≥ 70 years old age than in men ≥ 70 years old (16.2% vs 9.3%, respectively; p = 0.003) but was comparable between women and men in patients < 70 years old (5.7% vs 4.9%, respectively; p = 0.59). On multivariate analysis, the association between female gender and in-hospital mortality in patients ≥ 70 years old remained significant (odds ratio 1.78, 95% confidential interval 1.05 to 3.00), but the gender difference was not observed in patients < 70 years old (odds ratio 1.09, 95% confidence interval 0.53 to 2.24). In conclusion, female gender was associated with in-hospital mortality after acute myocardial infarction in patients ≥ 70 years old but not in patients < 70 years old. Copyright © 2011 Elsevier Inc. All rights reserved.

Development and validation of an instrument to assess patients' appraisal, emotions and action tendencies preceding care-seeking in acute myocardial infarction: The PA-AMI questionnaire.

PubMed

Nymark, C; Saboonchi, F; Mattiasson, A-C; Henriksson, P; Kiessling, A

2017-03-01

Reducing patient delay for patients afflicted by an acute myocardial infarction is a task of great complexity, which might be alleviated if more factors that influence this delay could be identified. Although a number of self-reported instruments associated with patient delay exist, none of these taps the content of the appraisal process related to patients' subjective emotions. The aim of this study was to develop and validate a questionnaire aimed at assessing patients' appraisal, emotions and action tendencies when afflicted by an acute myocardial infarction. An item pool was generated based on themes conceptualized in a recent qualitative study of acute myocardial infarction patients' thoughts, feelings and actions preceding the decision to seek medical care. The 'Think-Aloud Protocol' and test-retest analysis at item level were performed. The modified item pool was administered to 96 patients when treated for acute myocardial infarction. Explorative factor analysis and principal component analysis with the non-linear iterative partial least squares algorithm were performed to examine the underlying factor structure of the items. The findings indicated three core dimensions corresponding to three subscales, namely, 'symptom appraisal'; 'perceived inability to act'; 'autonomy preservation'. The results demonstrated acceptable measures of reliability and validity Conclusions: The PA-AMI questionnaire demonstrated satisfactory psychometric properties. Assessment of the included core dimensions may contribute to greater understanding of the appraisal processes for patients afflicted by an acute myocardial infarction.

MicroRNA-133 overexpression promotes the therapeutic efficacy of mesenchymal stem cells on acute myocardial infarction.

PubMed

Chen, Yueqiu; Zhao, Yunfeng; Chen, Weiqian; Xie, Lincen; Zhao, Zhen-Ao; Yang, Junjie; Chen, Yihuan; Lei, Wei; Shen, Zhenya

2017-11-25

Our study aim was to evaluate the therapeutic efficacy and mechanisms of miR-133-overexpressing mesenchymal stem cells (MSCs) on acute myocardial infarction. Rat MSCs were isolated and purified by whole bone marrow adherent culturing. After transfection with the agomir or antagomir of miR-133, MSCs were collected for assay of cell vitality, apoptosis, and cell cycle progression. At the same time, exosomes were isolated from the supernatant to analyze the paracrine miR-133. For in-vivo studies, constitutive activation of miR-133 in MSCs was achieved by lentivirus-mediated miR-133 overexpression. A rat myocardial infarction model was created by ligating the left anterior descending coronary artery, while control MSCs (vector-MSCs) or miR-133-overexpressed MSCs (miR-133-MSCs) were injected into the zone around the myocardial infarction. Subsequently, myocardial function was evaluated by echocardiography on days 7 and 28 post infarction. Finally the infarcted hearts were collected on days 7 and 28 for myocardial infarct size measurement and detection of snail 1 expression. Hypoxia-induced apoptosis of MSCs obviously reduced, along with enhanced expression of total poly ADP-ribose polymerase protein, after miR-133 agomir transfection, while the apoptosis rate increased in MSCs transfected with miR-133 antagomir. However, no change in cell viability and cell-cycle distribution was observed in control, miR-133-overexpressed, and miR-133-interfered MSCs. Importantly, rats transplanted with miR-133-MSCs displayed more improved cardiac function after acute myocardial infarction, compared with those that received vector-MSC injection. Further studies indicated that cardiac expression of snail 1 was significantly repressed by adjacent miR-133-overexpressing MSCs, and both the inflammatory level and the infarct size decreased in miR-133-MSC-injected rat hearts. miR-133-MSCs obviously improved cardiac function in a rat model of myocardial infarction. Transplantation of miR-133

[Renal dysfunction in patients with myocardial infarction concurrent with type 2 diabetes mellitus].

PubMed

Evseeva, M V; Karetnikova, V N; Barbarash, O L

2015-01-01

Carbohydrate metabolic disturbances are an independent risk factor for not only the development, but also poor course of cardiovascular diseases, particularly those concurrent with renal dysfunction (RD). This factor acquires particular relevance due to the fact that the incidence of type 2 diabetes mellitus significantly continues to rise worldwide. The review considers the main mechanisms and common components of the pathogenesis of RD, as well as the constituents forming its basis in the presence of carbohydrate metabolic disturbances. Moreover, it highlights the timely detection of RD, a search for new biomarkers of prognostic value for cardiovascular events, and the early diagnosis of RD. The review unveils the present view of optimal diagnostic and management tactics for patients with myocardial infarction concurrent with background diseases.

Health-related quality of life, sense of coherence and leisure-time physical activity in women after an acute myocardial infarction.

PubMed

Løvlien, Mona; Mundal, Liv; Hall-Lord, Marie-Louise

2017-04-01

To examine the relationship between leisure-time physical activity, health-related quality of life and sense of coherence in women after an acute myocardial infarction, and further to investigate whether these aspects were associated with age. Physical activity and health-related quality of life are vital aspects for patients after an acute myocardial infarction. Cross-sectional. All eligible women diagnosed with acute myocardial infarction received a postal questionnaire two to three months after hospital discharge, and 142 women were included. To measure health-related quality of life and sense of coherence, The MacNew Heart disease questionnaire and the Sense of coherence-13 scale was used. Respondents reporting at least one type of physical activity had significantly higher health-related quality of life as compared to respondents reporting no kind of physical activity. Respondents reporting physical activity for at least 30 minutes twice a week had significantly higher health-related quality of life scores than respondents being active less than twice a week. A weak association was found between physical activity level and sense of coherence. Reduction in physical activity after the acute myocardial infarction was associated with reduced health-related quality of life and sense of coherence. Sense of coherence was significantly associated with age, as respondents 75 years and older had significantly higher scores than respondents younger than 75 years. Physical activity, even at a low level, is significantly associated with increased health-related quality of life and to some extent to sense of coherence. Tailoring women after an acute myocardial infarction about lifestyle changes must include knowledge about the benefits of leisure-time physical activity, and that even a small amount of activity is associated with a better health-related quality of life. The utmost important assignment is to motivate the women for regular physical activity in their leisure

Could missile attacks trigger acute myocardial infarction?

PubMed

Zubaid, Mohammad; Suresh, Cheiyil G; Thalib, Lukman; Rashed, Wafa

2006-08-01

During the Gulf war in 2003, Kuwait was targeted with missile attacks for 10 consecutive days. Our objective is to evaluate the influence of missile attacks on the incidence of acute myocardial infarction (AMI). We retrospectively compared the number of admissions for AMI presenting to a major general hospital during missile attacks period (MAP) in 2003 with four control periods. MAP and each control period consisted of the same number of days (10 days). The four control periods were the 10 days immediately before and after MAP; and the same time period as MAP for the years 2001 and 2002. The number of admissions for AMI was highest during MAP, 21 cases compared to 14-16 cases in the four control periods, with a trend towards increase during MAP (incidence rate ratio = 1.59; 95% CI 0.95 to 2.66, p < 0.07). The number of admissions for AMI during the first 5 days of MAP was significantly higher compared to the first 5 days of the four control periods (incidence rate ratio = 2.43; 95% CI 1.23 to 4.26, p < 0.01). The observed AMI admission rate during the first 5 days of MAP was significantly higher than expected for a 5-day period in the years 2001, 2002 and 2003. This increase was specific to AMI and did not affect other acute cardiac conditions. Missile attacks were associated with an increase in the incidence of AMI. This increase was specific to AMI and did not influence acute cardiac conditions.

Review of Acute Coronary Syndromes: Diagnosis and Management of ST-Elevation Myocardial Infarction.

PubMed

Yee, Jimmy; Rajpurohit, Naveen; Khan, Muhammad A; Stys, Adam

2015-08-01

Acute coronary syndrome is a life-threatening event that affects millions of people each year and accounts for a big portion of hospital visits. With an ever-growing elderly patient population, ischemic heart disease is more prevalent than ever before. It is paramount that physicians of all fields are cognizant of the various presentations of acute coronary syndrome (ACS), as its prompt diagnosis and treatment profoundly decreases mortality and morbidity. Under the American College of Cardiology Foundation and the American Heart Association, guidelines are published for the optimal management of patients with acute coronary syndromes. Guidelines are continuously evolving as more multicenter randomized trials, new medications and new technologies continue to change the way we treat acute coronary syndromes. The focus of this review is ST-elevation myocardial infarction and it provides answers to some of the fundamental questions through evidence-based guidelines.

Role of CD11b+Gr-1+ myeloid cells in AGEs-induced myocardial injury in a mice model of acute myocardial infarction.

PubMed

Yao, Tongqing; Lu, Wenbin; Zhu, Jian; Jin, Xian; Ma, Genshan; Wang, Yuepeng; Meng, Shu; Zhang, Yachen; Li, Yigang; Shen, Chengxing

2015-01-01

Polymorph neutrophils are the predominant inflammatory cells and play a crucial role on the pathogenesis of myocardial injury at the early stage of acute myocardial infarction (AMI). However, the precursors and the differentiation of neutrophils are not fully understood. Here we explored the role of CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) on myocardial injury in the absence and presence of advanced glycation end-products (AGEs) in a mice model of AMI. Male C57BL/6J mice were selected. Fluorescent actived cell sortor (FACS) data demonstrated significantly increased CD11b+Gr-1+ MDSCs both in peripheral blood circulation and in the ischemic myocardium at 24 hours post AMI. Quantitative-real-time PCR results also revealed significantly upregulated CD11b and Ly6G mRNA expression in the ischemic myocardium. AGEs treatment further aggravated these changes in AMI mice but not in sham mice. Moreover, AGEs treatment also significantly increased infarction size and enhanced cardiomyocyte apoptosis. The mRNA expression of pro-inflammatory cytokine IL-6 and iNOS2 was also significantly increased in AMI + AGEs group compared to AMI group. These data suggest enhanced infiltration of MDSCs by AGEs contributes to aggravated myocardial injury in AMI mice, which might be one of the mechanisms responsible for severer myocardial injury in AMI patients complicating diabetes.

Extreme Right Axis Deviation in Acute Myocardial Infarction: A Hazardous Signal of Poor Prognosis.

PubMed

Wang, Qingyu; Pan, Shuo; Liu, Fuqiang; Yang, Dan; Wang, Jun-Kui

2018-05-11

BACKGROUND New-onset extreme right axis deviation and right bundle branch block (RBBB) are rare during acute myocardial infarction (AMI), and has only been reported in several cases reflecting the severity of AMI. It could predict severe clinical complications and higher risks in coronary artery disease. Although there is little electrophysiological explanation, the complications are severe. They should be emphasized in newly diagnosed extreme right axis deviation and RBBB in AMI. CASE REPORT A 72-year-old male was admitted to our department with a chief complaint of intermittent retrosternal chest pain and was diagnosed with extensive anterior myocardial infarction with RBBB, by elevated myocardial enzymes and ECG. The main wave direction of QRS in lead aVR was positive and showed an extreme right axis deviation. After a month, the patient's chest distress and the RBBB vanished, but a right axis deviation still existed. The echocardiogram showed prior extensive anterior myocardial infarction (including apex myocardia) and lower LVEF. CONCLUSIONS New diagnosed RBBB and right axis deviation is uncommon and could be a useful clue to evaluate myocardial ischemia in AMI cases. This electrocardiographic marker can identify coronary artery occlusion where ST-segments are hard to evaluate, and hence, patients may benefit most from early and complete revascularization strategies such as primary angioplasty.

Inequality in treatment use among elderly patients with acute myocardial infarction: USA, Belgium and Quebec.

PubMed

Perelman, Julian; Shmueli, Amir; McDonald, Kathryn M; Pilote, Louise; Saynina, Olga; Closon, Marie-Christine

2009-07-30

Previous research has provided evidence that socioeconomic status has an impact on invasive treatments use after acute myocardial infarction. In this paper, we compare the socioeconomic inequality in the use of high-technology diagnosis and treatment after acute myocardial infarction between the US, Quebec and Belgium paying special attention to financial incentives and regulations as explanatory factors. We examined hospital-discharge abstracts for all patients older than 65 who were admitted to hospitals during the 1993-1998 period in the US, Quebec and Belgium with a primary diagnosis of acute myocardial infarction. Patients' income data were imputed from the median incomes of their residential area. For each country, we compared the risk-adjusted probability of undergoing each procedure between socioeconomic categories measured by the patient's area median income. Our findings indicate that income-related inequality exists in the use of high-technology treatment and diagnosis techniques that is not justified by differences in patients' health characteristics. Those inequalities are largely explained, in the US and Quebec, by inequalities in distances to hospitals with on-site cardiac facilities. However, in both Belgium and the US, inequalities persist among patients admitted to hospitals with on-site cardiac facilities, rejecting the hospital location effect as the single explanation for inequalities. Meanwhile, inequality levels diverge across countries (higher in the US and in Belgium, extremely low in Quebec). The findings support the hypothesis that income-related inequality in treatment for AMI exists and is likely to be affected by a country's system of health care.

Vasospasm of atherosclerotic coronary arteries precipitates acute ischemic myocardial damage in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits.

PubMed

Shiomi, Masashi; Ishida, Tatsuro; Kobayashi, Tsutomu; Nitta, Norihisa; Sonoda, Akinaga; Yamada, Satoshi; Koike, Tomonari; Kuniyoshi, Nobue; Murata, Kiyoshi; Hirata, Ken-ichi; Ito, Takashi; Libby, Peter

2013-11-01

This study tested the hypothesis that vasospasm can trigger coronary plaque injury and acute ischemic myocardial damage. Myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits received an intravenous bolus of ergonovine maleate (0.45 µmol/kg) during intravenous infusion of norepinephrine (12 nmol/kg per minute) to provoke coronary spasm in vivo. After this treatment, coronary angiography demonstrated vasospasm, and the ECG showed ischemic abnormalities (ST depression/elevation and T-wave inversion) in 77% of animals (23/30). These changes normalized after nitroglycerin injection. In rabbits that demonstrated these ECG findings for >20 minutes, echocardiograms showed left ventricular wall motion abnormality. Serum levels of heart-type fatty acid-binding protein, cardiac troponin-I, and myoglobin increased markedly 4 hours after spasm provocation. In coronary lesions of myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits with provoked coronary spasm, we observed intimal injury in 60.9% in the form of endothelial cell protrusions (39.1%), denudation (30.4%), and macrophage extravasation (56.5%). Plaque disruption with luminal thrombus, however, was only seen in 2 of 23 animals (8.7%), and mural microthrombus was rarely observed (4.3%). These observations show that provocation of vasospasm in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits associates with subsequent ischemic myocardial damage. Although treatment with spasmogens altered aspects of plaque morphology, for example, endothelial protrusion and macrophage emigration, thrombosis was rare in these animals with chronic atherosclerotic disease.

Microvascular resistance of the culprit coronary artery in acute ST-elevation myocardial infarction

PubMed Central

Carrick, David; Haig, Caroline; Carberry, Jaclyn; McCartney, Peter; Welsh, Paul; Ahmed, Nadeem; McEntegart, Margaret; Petrie, Mark C.; Eteiba, Hany; Lindsay, Mitchell; Hood, Stuart; Watkins, Stuart; Rauhalammi, Samuli M.O.; Mordi, Ify; Ford, Ian; Radjenovic, Aleksandra; Sattar, Naveed; Oldroyd, Keith G.

2016-01-01

BACKGROUND. Failed myocardial reperfusion is common and prognostically important after acute ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate coronary flow reserve (CFR), a measure of vasodilator capacity, and the index of microvascular resistance (IMR; mmHg × s) in the culprit artery of STEMI survivors. METHODS. IMR (n = 288) and CFR (n = 283; mean age [SD], 60 [12] years) were measured acutely using guide wire–based thermodilution. Cardiac MRI disclosed left ventricular pathology, function, and volumes at 2 days (n = 281) and 6 months after STEMI (n = 264). All-cause death or first heart failure hospitalization was independently adjudicated (median follow-up 845 days). RESULTS. Myocardial hemorrhage and microvascular obstruction occurred in 89 (42%) and 114 (54%) patients with evaluable T2*-MRI maps. IMR and CFR were associated with microvascular pathology (none vs. microvascular obstruction only vs. microvascular obstruction and myocardial hemorrhage) (median [interquartile range], IMR: 17 [12.0–33.0] vs. 17 [13.0–39.0] vs. 37 [21.0–63.0], P < 0.001; CFR: 1.7 [1.4–2.5] vs. 1.5 [1.1–1.8] vs. 1.4 [1.0–1.8], P < 0.001), whereas thrombolysis in myocardial infarction blush grade was not. IMR was a multivariable associate of changes in left ventricular end-diastolic volume (regression coefficient [95% CI] 0.13 [0.01, 0.24]; P = 0.036), whereas CFR was not (P = 0.160). IMR (5 units) was a multivariable associate of all-cause death or heart failure hospitalization (n = 30 events; hazard ratio [95% CI], 1.09 [1.04, 1.14]; P < 0.001), whereas CFR (P = 0.124) and thrombolysis in myocardial infarction blush grade (P = 0.613) were not. IMR had similar prognostic value for these outcomes as <50% ST-segment resolution on the ECG. CONCLUSIONS. IMR is more closely associated with microvascular pathology, left ventricular remodeling, and health outcomes than the angiogram or CFR. TRIAL REGISTRATION. NCT02072850. FUNDING. A

Left Ventricular Free Wall Rupture in Acute Myocardial Infarction

PubMed Central

Amir, Offer; Smith, Ronald; Nishikawa, Akaira; Gregoric, Igor D.; Smart, Frank W.

2005-01-01

We describe a case of subacute left ventricular free wall rupture during acute myocardial infarction in a 68-year-old man. The diagnosis was confirmed by echocardiography. The patient was supported by an intra-aortic balloon pump until the ruptured wall could be successfully repaired by suturing and gluing a pericardial patch over the defect and bypassing the left anterior descending coronary artery with a vein graft. This case demonstrates that left ventricular free wall rupture is not always fatal and that early diagnosis and institution of intra-aortic balloon pump support in such patients can allow successful bridging to definitive emergency surgical therapy. PMID:16392235

Sex differences in perceived stress and early recovery in young and middle-aged patients with acute myocardial infarction.

PubMed

Xu, Xiao; Bao, Haikun; Strait, Kelly; Spertus, John A; Lichtman, Judith H; D'Onofrio, Gail; Spatz, Erica; Bucholz, Emily M; Geda, Mary; Lorenze, Nancy P; Bueno, Héctor; Beltrame, John F; Krumholz, Harlan M

2015-02-17

Younger age and female sex are both associated with greater mental stress in the general population, but limited data exist on the status of perceived stress in young and middle-aged patients presenting with acute myocardial infarction. We examined sex difference in stress, contributing factors to this difference, and whether this difference helps explain sex-based disparities in 1-month recovery using data from 3572 patients with acute myocardial infarction (2397 women and 1175 men) 18 to 55 years of age. The average score of the 14-item Perceived Stress Scale at baseline was 23.4 for men and 27.0 for women (P<0.001). Higher stress in women was explained largely by sex differences in comorbidities, physical and mental health status, intrafamily conflict, caregiving demands, and financial hardship. After adjustment for demographic and clinical characteristics, women had worse recovery than men at 1 month after acute myocardial infarction, with mean differences in improvement score between women and men ranging from -0.04 for EuroQol utility index to -3.96 for angina-related quality of life (P<0.05 for all). Further adjustment for baseline stress reduced these sex-based differences in recovery to -0.03 to -3.63, which, however, remained statistically significant (P<0.05 for all). High stress at baseline was associated with significantly worse recovery in angina-specific and overall quality of life, as well as mental health status. The effect of baseline stress on recovery did not vary between men and women. Among young and middle-aged patients, higher stress at baseline is associated with worse recovery in multiple health outcomes after acute myocardial infarction. Women perceive greater psychological stress than men at baseline, which partially explains women's worse recovery. © 2015 American Heart Association, Inc.

Patent foramen ovale increases the risk of acute ischemic stroke in patients with acute pulmonary embolism leading to right ventricular dysfunction.

PubMed

Goliszek, Sylwia; Wiśniewska, Małgorzata; Kurnicka, Katarzyna; Lichodziejewska, Barbara; Ciurzyński, Michał; Kostrubiec, Maciej; Gołębiowski, Marek; Babiuch, Marek; Paczynska, Marzanna; Koć, Marcin; Palczewski, Piotr; Wyzgał, Anna; Pruszczyk, Piotr

2014-11-01

Patent foramen ovale (PFO) is an established risk factor for ischemic stroke. Since acute right ventricular dysfunction (RVD) observed in patients with PE can lead to right-to-left inter-atrial shunt via PFO, we hypothesized that PFO is a risk factor for ischemic stroke in PE with significant right ventricular dysfunction. 55 patients (31 F, 24M), median age 49 years (range 19-83 years) with confirmed PE underwent echocardiography for RVD and PFO assessment. High risk acute PE was diagnosed in 3 (5.5%) patients, while 16 (29%) hemodynamically stable with RVD patients formed a group with intermediate-risk PE. PFO was diagnosed in 19 patients (34.5%). Diffusion-weighted MRI of the brain for acute ischemic stroke (AIS) was performed in all patients 4.91 ± 4.1 days after admission. AIS was detected by MRI in 4 patients (7.3%). Only one stroke was clinically overt and resulted in hemiplegia. All 4 AIS occurred in the PFO positive group (4 of 19 patients), and none in subjects without PFO (21.0% vs 0%, p=0.02). Moreover, all AIS occurred in patients with RVD and PFO, and none in patients with PFO without RVD (50% vs 0%, p=0.038). Our data suggest that acute pulmonary embolism resulting in right ventricular dysfunction may lead to acute ischemic stroke in patients with patent foramen ovale. However, the clinical significance of such lesions remains to be determined. Copyright © 2014 Elsevier Ltd. All rights reserved.

Adenoviral short hairpin RNA therapy targeting phosphodiesterase 5a relieves cardiac remodeling and dysfunction following myocardial infarction.

PubMed

Li, Longhu; Haider, Husnain Kh; Wang, Linlin; Lu, Gang; Ashraf, Muhammad

2012-05-15

We previously showed that treatment with tadalafil, a long-acting phosphodiesterase-5a (PDE5a) inhibitor, effectively prevented adverse left ventricular (LV) remodeling of the infarcted heart. We hypothesized that short-hairpin RNA (shRNA) therapy targeting PDE5a would simulate the effects of pharmacological intervention for treatment of postinfarction LV remodeling and dysfunction. Experimental model of myocardial infarction was developed in female mice by permanent ligation of left coronary artery. Immediately after that, an adenoviral vector encoding for shRNA sequence targeting PDE5a (Ad-shPDE5a) was injected intramyocardially, which specifically inhibited PDE5a in the heart. Four weeks later, Ad-shPDE5a treated mice showed significant mitigation of the left ventricle (LV) dilatation and dysfunction as indicated by smaller LV cavity and more preserved ejection fraction and fractional shortening. Infarction size and fibrosis were significantly reduced in Ad-shPDE5a-treated mice. Additionally, more salvaged cardiomyocytes, significantly reduced collagen contents, and higher blood vessel density were observed in Ad-shPDE5a-treated mice. The cytoprotective effects of Ad-shPDE5a were demonstrated in vitro in Ad-shPDE5a transfected cardiomyocytes cultured under oxygen glucose deprivation. Among downstream mediators of PDE5a signaling, cyclic GMP (cGMP) and cGMP-dependent protein kinase G (PKG) were activated with concomitant reduction in caspase-3 activity. However, no significant change in PKA and cAMP activities were observed in Ad-shPDE5a-treated hearts. Inhibition with shRNA improved cardiac remodeling and dysfunction by reducing infarction size and cardiac fibrosis and increased cGMP and PKG activity. These findings suggest that PDE5 inhibition with Ad-shPDE5a is a novel approach for treatment of myocardial infarction.

IGF-1 Alleviates High Fat Diet-Induced Myocardial Contractile Dysfunction: Role of Insulin Signaling and Mitochondrial Function

PubMed Central

Zhang, Yingmei; Yuan, Ming; Bradley, Katherine M.; Dong, Feng; Anversa, Piero; Ren, Jun

2012-01-01

Obesity is often associated with reduced plasma IGF-1 levels, oxidative stress, mitochondrial damage and cardiac dysfunction. This study was designed to evaluate the impact of IGF-1 on high fat diet-induced oxidative, myocardial, geometric and mitochondrial responses. FVB and cardiomyocyte-specific IGF-1 overexpression transgenic mice were fed a low (10%) or high fat (45%) diet to induce obesity. High fat diet feeding led to glucose intolerance, elevated plasma levels of leptin, interleukin-6, insulin and triglyceride as well as reduced circulating IGF-1 levels. Echocardiography revealed reduced fractional shortening, increased end systolic and diastolic diameter, increased wall thickness, and cardiac hypertrophy in high fat-fed FVB mice. High fat diet promoted ROS generation, apoptosis, protein and mitochondrial damage, reduced ATP content, cardiomyocyte cross-sectional area, contractile and intracellular Ca2+ dysregulation, including depressed peak shortening and maximal velocity of shortening/relengthening, prolonged duration of relengthening, and dampened intracellular Ca2+ rise and clearance. Western blot analysis revealed disrupted phosphorylation of insulin receptor, post-receptor signaling molecules IRS-1 (tyrosine/serine phosphorylation), Akt, GSK3β, Foxo3a, mTOR, as well as downregulated expression of mitochondrial proteins PPARγ coactivator 1α (PGC1α) and UCP-2. Intriguingly, IGF-1 mitigated high fat diet feeding-induced alterations in ROS, protein and mitochondrial damage, ATP content, apoptosis, myocardial contraction, intracellular Ca2+ handling and insulin signaling, but not whole body glucose intolerance and cardiac hypertrophy. Exogenous IGF-1 treatment also alleviated high fat diet-induced cardiac dysfunction. Our data revealed that IGF-1 alleviates high fat diet-induced cardiac dysfunction despite persistent cardiac remodeling, possibly due to preserved cell survival, mitochondrial function and insulin signaling. PMID:22275536

Adenoviral short hairpin RNA therapy targeting phosphodiesterase 5a relieves cardiac remodeling and dysfunction following myocardial infarction

PubMed Central

Li, Longhu; Haider, Husnain Kh.; Wang, Linlin; Lu, Gang

2012-01-01

We previously showed that treatment with tadalafil, a long-acting phosphodiesterase-5a (PDE5a) inhibitor, effectively prevented adverse left ventricular (LV) remodeling of the infarcted heart. We hypothesized that short-hairpin RNA (shRNA) therapy targeting PDE5a would simulate the effects of pharmacological intervention for treatment of postinfarction LV remodeling and dysfunction. Experimental model of myocardial infarction was developed in female mice by permanent ligation of left coronary artery. Immediately after that, an adenoviral vector encoding for shRNA sequence targeting PDE5a (Ad-shPDE5a) was injected intramyocardially, which specifically inhibited PDE5a in the heart. Four weeks later, Ad-shPDE5a treated mice showed significant mitigation of the left ventricle (LV) dilatation and dysfunction as indicated by smaller LV cavity and more preserved ejection fraction and fractional shortening. Infarction size and fibrosis were significantly reduced in Ad-shPDE5a-treated mice. Additionally, more salvaged cardiomyocytes, significantly reduced collagen contents, and higher blood vessel density were observed in Ad-shPDE5a-treated mice. The cytoprotective effects of Ad-shPDE5a were demonstrated in vitro in Ad-shPDE5a transfected cardiomyocytes cultured under oxygen glucose deprivation. Among downstream mediators of PDE5a signaling, cyclic GMP (cGMP) and cGMP-dependent protein kinase G (PKG) were activated with concomitant reduction in caspase-3 activity. However, no significant change in PKA and cAMP activities were observed in Ad-shPDE5a-treated hearts. Inhibition with shRNA improved cardiac remodeling and dysfunction by reducing infarction size and cardiac fibrosis and increased cGMP and PKG activity. These findings suggest that PDE5 inhibition with Ad-shPDE5a is a novel approach for treatment of myocardial infarction. PMID:22447941

Cardioprotective effects of traditional Chinese medicine Guanmaitong on acute myocardial infarction.

PubMed

Wang, Xing-Hua; Li, Guang-Ping; Yang, Wan-Song; Jiao, Zhan-Quan; Liu, Hong-Mei; Ni, Yan-Ping

2016-12-01

Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI). Sprague-Dawley rats were randomly allocated into five groups: Control group (sham-operated), the model group, and small, medium, and large dosage GMT groups. The rat model of AMI was established via ligation of the coronary artery. The results indicate that GMT was able to reduce myocardial infarction size and improve the activities of tumor necrosis factor-α (TNF-α), intercellular adhesion molecule 1 (ICAM-1) and interleukin-1. Furthermore, the reduced apoptotic index of the GMT-treated cardiocytes (P<0.05 vs. model group) was in accordance with the downregulated expression of Bax and the upregulated expression of Bcl-2. In conclusion, GMT may exert a protective potential against myocardial infarction injury by inhibiting apoptosis and inflammation of cardiomyocytes, and may offer a promising adjunct treatment for CHD.

Cardioprotective effects of traditional Chinese medicine Guanmaitong on acute myocardial infarction

PubMed Central

Wang, Xing-Hua; Li, Guang-Ping; Yang, Wan-Song; Jiao, Zhan-Quan; Liu, Hong-Mei; Ni, Yan-Ping

2016-01-01

Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI). Sprague-Dawley rats were randomly allocated into five groups: Control group (sham-operated), the model group, and small, medium, and large dosage GMT groups. The rat model of AMI was established via ligation of the coronary artery. The results indicate that GMT was able to reduce myocardial infarction size and improve the activities of tumor necrosis factor-α (TNF-α), intercellular adhesion molecule 1 (ICAM-1) and interleukin-1. Furthermore, the reduced apoptotic index of the GMT-treated cardiocytes (P<0.05 vs. model group) was in accordance with the downregulated expression of Bax and the upregulated expression of Bcl-2. In conclusion, GMT may exert a protective potential against myocardial infarction injury by inhibiting apoptosis and inflammation of cardiomyocytes, and may offer a promising adjunct treatment for CHD. PMID:28105124

Tissue Doppler imaging for detection of radial and longitudinal myocardial dysfunction in a family of cats affected by dystrophin-deficient hypertrophic muscular dystrophy.

PubMed

Chetboul, Valérie; Blot, Stephane; Sampedrano, Carolina Carlos; Thibaud, Jean-Laurent; Granger, Nicolas; Tissier, Renaud; Bruneval, Patrick; Gaschen, Frederic; Gouni, Vassiliki; Nicolle, Audrey P; Pouchelon, Jean-Louis

2006-01-01

Diagnosis of feline hypertrophic cardiomyopathy currently is based on the presence of myocardial hypertrophy detected using conventional echocardiography. The accuracy of tissue Doppler imaging (TDI) for earlier detection of the disease has never been described. The objective of this sudy was to quantify left ventricular free wall (LVFW) velocities in cats with hypertrophic muscular dystrophy (HFMD) during preclinical cardiomyopathy using TDI. The study animals included 22 healthy controls and 7 cats belonging to a family of cats with HFMD (2 affected adult males, 2 heterozygous adult females, one 2.5-month-old affected male kitten, and 2 phenotypically normal female kittens from the same litter). All cats were examined via conventional echocardiography and 2-dimensional color TDI. No LVFW hypertrophy was detected in the 2 carriers or in the affected kitten when using conventional echocardiography and histologic examination, respectively. The LVFW also was normal for 1 affected male and at the upper limit of normal for the 2nd male. Conversely, LVFW dysfunction was detected in all affected and carrier cats with HFMD when using TDI. TDI consistently detects LVFW dysfunction in cats with HFMD despite the absence of myocardial hypertrophy. Therefore, TDI appears more sensitive than conventional echocardiography in detecting regional myocardial abnormalities.

Impact of the Metabolic Syndrome on the Clinical Outcome of Patients with Acute ST-Elevation Myocardial Infarction

PubMed Central

Lee, Min Goo; Ahn, Youngkeun; Chae, Shung Chull; Hur, Seung Ho; Hong, Taek Jong; Kim, Young Jo; Seong, In Whan; Chae, Jei Keon; Rhew, Jay Young; Chae, In Ho; Cho, Myeong Chan; Bae, Jang Ho; Rha, Seung Woon; Kim, Chong Jin; Choi, Donghoon; Jang, Yang Soo; Yoon, Junghan; Chung, Wook Sung; Cho, Jeong Gwan; Seung, Ki Bae; Park, Seung Jung

2010-01-01

We sought to determine the prevalence of metabolic syndrome (MS) in patients with acute myocardial infarction and its effect on clinical outcomes. Employing data from the Korea Acute Myocardial Infarction Registry, a total of 1,990 patients suffered from acute ST-elevation myocardial infarction (STEMI) between November 2005 and December 2006 were categorized according to the National Cholesterol Education Program-Adult Treatment Panel III criteria of MS. Primary study outcomes included major adverse cardiac events (MACE) during one-year follow-up. Patients were grouped based on existence of MS: group I: MS (n=1,182, 777 men, 62.8±12.3 yr); group II: Non-MS (n=808, 675 men, 64.2±13.1 yr). Group I showed lower left ventricular ejection fraction (LVEF) (P=0.005). There were no differences between two groups in the coronary angiographic findings except for multivessel involvement (P=0.01). The incidence of in-hospital death was higher in group I than in group II (P=0.047), but the rates of composite MACE during one-year clinical follow-up showed no significant differences. Multivariate analysis showed that low LVEF, old age, MS, low high density lipoprotein cholesterol and multivessel involvement were associated with high in-hospital death rate. In conclusion, MS is an important predictor for in-hospital death in patients with STEMI. PMID:20890426

Effects of Combined Milrinone and Levosimendan Treatment on Systolic and Diastolic Function During Postischemic Myocardial Dysfunction in a Porcine Model.

PubMed

Axelsson, Birger; Häggmark, Sören; Svenmarker, Staffan; Johansson, Göran; Gupta, Anil; Tydén, Hans; Wouters, Patrick; Haney, Michael

2016-09-01

It is not known whether there are positive or negative interactions on ventricular function when a calcium-sensitizing inotrope is added to a phosphodiesterase inhibitor in the clinical setting of acute left ventricular (LV) dysfunction. We hypothesized that when levosimendan is added to milrinone treatment, there will be synergetic inotropic and lusitropic effects. This was tested in an anesthetized porcine postischemic global LV injury model, where ventricular pressures and volumes (conductance volumetry) were measured. A global ischemic injury was induced by repetitive left main stem coronary artery occlusions. Load-independent indices of LV function were assessed before and after ventricular injury, after milrinone treatment, and finally after addition of levosimendan to the milrinone treatment. Nonparametric, within-group comparisons were made. The protocol was completed in 12 pigs, 7 of which received the inotrope treatment and 5 of which served as controls. Milrinone led to positive lusitropic effects seen by improvement in tau after myocardial stunning. The addition of levosimendan to milrinone further increased lusitropic state. The latter effect could however not be attributed solely to levosimendan, since lusitropic state also improved spontaneously in time-matched controls at the same rate during the corresponding period. When levosimendan was added to milrinone infusion, there was no increase in systolic function (preload recruitable stroke work) compared to milrinone treatment alone. We conclude that in this model of postischemic LV dysfunction, there appears to be no clear improvement in systolic or diastolic function after addition of levosimendan to established milrinone treatment but also no negative effects of levosimendan in this context. © The Author(s) 2016.

Successful use of high-dose cytarabine in a patient with acute myeloid leukemia and severe hepatic dysfunction.

PubMed

Barker, Jacob A; Marini, Bernard L; Bixby, Dale; Perissinotti, Anthony J

2016-12-01

Acute myeloid leukemia is a hematologic malignancy characterized by the clonal expansion of myeloid blasts in the peripheral blood, bone marrow, and other tissues. Prognosis is poor with 5-year survival rates ranging from 5-65% depending on demographic and clinical features. Outcomes are worse for patients that have an antecedent myeloproliferative neoplasm that evolves to acute myeloid leukemia, with a survival rate of <10%. Treatment for acute myeloid leukemia has remained cytarabine and an anthracycline given in the standard 3 + 7 regimen. However, for patients with liver dysfunction this regimen, among many others, cannot be given safely. There is currently a lack of data regarding the use of cytarabine in patients with severe hepatic dysfunction. In this case report, we present a patient with secondary acute myeloid leukemia who successfully received a modified regimen of high-dose cytarabine while in severe hepatic dysfunction (bilirubin >15 mg/dL). © The Author(s) 2015.

Assessment of dyssynchronous wall motion during acute myocardial ischemia using velocity vector imaging.

PubMed

Masuda, Kasumi; Asanuma, Toshihiko; Taniguchi, Asuka; Uranishi, Ayumi; Ishikura, Fuminobu; Beppu, Shintaro

2008-03-01

The purpose of this study was to investigate the diagnostic value of velocity vector imaging (VVI) for detecting acute myocardial ischemia and whether VVI can accurately demonstrate the spatial extent of ischemic risk area. Using a tracking algorithm, VVI can display velocity vectors of regional wall motion overlaid onto the B-mode image and allows the quantitative assessment of myocardial mechanics. However, its efficacy for diagnosing myocardial ischemia has not been evaluated. In 18 dogs with flow-limiting stenosis and/or total occlusion of the coronary artery, peak systolic radial velocity (V(SYS)), radial velocity at mitral valve opening (V(MVO)), peak systolic radial strain, and the percent change in wall thickening (%WT) were measured in the normal and risk areas and compared to those at baseline. Sensitivity and specificity for detecting the stenosis and occlusion were analyzed in each parameter. The area of inward velocity vectors at mitral valve opening (MVO) detected by VVI was compared to the risk area derived from real-time myocardial contrast echocardiography (MCE). Twelve image clips were randomly selected from the baseline, stenosis, and occlusions to determine the intra- and inter-observer agreement for the VVI parameters. The left circumflex coronary flow was reduced by 44.3 +/- 9.0% during stenosis and completely interrupted during occlusion. During coronary artery occlusion, inward motion at MVO was observed in the risk area. Percent WT, peak systolic radial strain, V(SYS), and V(MVO) changed significantly from values at baseline. During stenosis, %WT, peak systolic radial strain, and V(SYS) did not differ from those at baseline; however, V(MVO) was significantly increased (-0.12 +/- 0.60 cm/s vs. -0.96 +/- 0.55 cm/s, p = 0.015). Sensitivity and specificity of V(MVO) for detecting ischemia were superior to those of other parameters. The spatial extent of inward velocity vectors at MVO correlated well with that of the risk area derived from MCE

"Spice" (Synthetic Marijuana) Induced Acute Myocardial Infarction: A Case Series.

PubMed

Ul Haq, E; Shafiq, A; Khan, A A; Awan, A A; Ezad, S; Minteer, W J; Omar, B

2017-01-01

Marijuana is the most widely abused "recreational" substance in the United States, with highest prevalence in young adults. It is reported to cause ischemic strokes, hepatitis, anxiety, and psychosis. Although it is associated with dose dependent tachycardia and can lead to coronary vasospasm, it has not been directly related to acute myocardial infarction (AMI). Marijuana induced coronary vasospasm can result in endothelial denudation at the site of a vulnerable atherosclerotic plaque in response to hemodynamic stressors, potentially causing an AMI. Spice refers to herbal mixture with composition and effects similar to that of marijuana and therefore is referred to as "synthetic marijuana." Herein, we report 3 cases of spice induced ST-segment elevation myocardial infarction. All patients were relatively young and had few or absolutely no risk factors for cardiovascular disease. All patients underwent emergent coronary angiography, with two needing stent placement and the third requiring only aspiration thrombectomy. Our case series emphasizes the importance of suspecting and investigating synthetic marijuana use in low risk young adults presenting with AMI.

Autonomic Dysfunction Predicts Clinical Outcomes After Acute Ischemic Stroke: A Prospective Observational Study.

PubMed

Xiong, Li; Tian, Ge; Leung, Howan; Soo, Yannie O Y; Chen, Xiangyan; Ip, Vincent H L; Mok, Vincent C T; Chu, Winnie C W; Wong, Ka Sing; Leung, Thomas W H

2018-01-01

Central autonomic dysfunction increases stroke morbidity and mortality. We aimed to investigate whether poststroke autonomic dysfunction graded by Ewing battery can predict clinical outcome. In this prospective observational study, we assessed autonomic function of ischemic stroke patients within 7 days from symptom onset by Ewing battery. On the basis of the magnitude of autonomic dysfunction, we stratified patients into significant (definite, severe, or atypical) or minor (normal or early) autonomic function impairment groups and correlated the impairment with the 3-month modified Rankin Scale score (good outcome: modified Rankin Scale score 0≈2; poor outcome: modified Rankin Scale score 3≈6). Among the 150 patients enrolled (mean age, 66.4±9.9 years; 70.7% males), minor autonomic dysfunction was identified in 36 patients (24.0%), and significant autonomic dysfunction was identified in 114 patients (76.0%) based on Ewing battery. In 3 months, a poor functional outcome was found in 32.5% of significant group patients compared with 13.9% in the minor group ( P =0.031). Crude odds ratios of the magnitude of autonomic dysfunction and 3-month unfavorable functional outcome after acute ischemic stroke were 2.979 (95% confidence interval, 1.071-8.284; P =0.036). After adjusting for confounding variables with statistical significance between the 2 functional outcome subgroups identified in univariate analysis (including sex and National Institutes of Health Stroke Scale score on admission), the magnitude of autonomic dysfunction still independently predicted an unfavorable outcome, with an odds ratio of 3.263 (95% confidence interval, 1.141-9.335; P =0.027). Autonomic dysfunction gauged by Ewing battery predicts poor functional outcome after acute ischemic stroke. © 2017 American Heart Association, Inc.

Acute insulin resistance in ST-segment elevation myocardial infarction in non-diabetic patients is associated with incomplete myocardial reperfusion and impaired coronary microcirculatory function

PubMed Central

2014-01-01

Background Insulin resistance (IR) assessed by the Homeostatic Model Assessment (HOMA) index in the acute phase of myocardial infarction in non-diabetic patients was recently established as an independent predictor of intrahospital mortality. In this study we postulated that acute IR is a dynamic phenomenon associated with the development of myocardial and microvascular injury and larger final infarct size in patients with ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (pPCI). Methods In 104 consecutive patients with the first anterior STEMI without diabetes, the HOMA index was determined on the 2nd and 7th day after pPCI. Worst-lead residual ST-segment elevation (ST-E) on postprocedural ECG, coronary flow reserve (CFR) determined by transthoracic Doppler echocardiography on the 2nd day after pPCI and fixed perfusion defect on single-photon emission computed tomography myocardial perfusion imaging (SPECT-MPI) determined six weeks after pPCI were analyzed according to HOMA indices. Results IR was present in 55 % and 58 % of patients on day 2 and day 7, respectively. Incomplete post-procedural ST-E resolution was more frequent in patients with IR compared to patients without IR, both on day 2 (p = 0.001) and day 7 (p < 0.001). The HOMA index on day 7 correlated with SPECT-MPI perfusion defect (r = 0.331), whereas both HOMA indices correlated well with CFR (r = -0.331 to -0.386) (p < 0.01 for all). In multivariable backward logistic regression analysis adjusted for significant univariate predictors and potential confounding variables, IR on day 2 was an independent predictor of residual ST-E ≥ 2 mm (OR 11.70, 95% CI 2.46-55.51, p = 0.002) and CFR < 2 (OR = 5.98, 95% CI 1.88-19.03, p = 0.002), whereas IR on day 7 was an independent predictor of SPECT-MPI perfusion defect > 20% (OR 11.37, 95% CI 1.34-96.21, p = 0.026). Conclusion IR assessed by the HOMA index during the

Organization of Care for Acute Myocardial Infarction in Rural and Urban Hospitals in Kansas

ERIC Educational Resources Information Center

Ellerbeck, Edward F.; Bhimaraj, Arvind; Perpich, Denise

2004-01-01

One in 4 Americans lives in a rural community and relies on rural hospitals and medical systems for emergent care of acute myocardial infarctions (AMI). The infrastructure and organization of AMI care in rural and urban Kansas hospitals was examined. Using a nominal group process, key elements within hospitals that might influence quality of AMI…

Reductions in Cigarette Smoking and Acute Myocardial Infarction Mortality in Jefferson County, Texas

PubMed Central

Huang, Philip; Ramirez, Amelie G.; Harrist, Ronald B.; Fonseca, Vincent P.

2010-01-01

After litigation against the tobacco industry ended in a settlement, the Texas legislature funded pilot projects to reduce tobacco use in selected areas of the state. Subsequent telephone surveys showed that well-funded activities were successful in reducing population rates of self-reported cigarette smoking. We present evidence that the reduction in smoking promptly led to lower rates of death from acute myocardial infarctions. PMID:20966365

Acute triggers of myocardial infarction: A case-crossover study.

PubMed

Ghiasmand, Maryam; Moghadamnia, Mohammad Taghi; Pourshaikhian, Majid; Kazemnejad Lili, Ehsan

2017-12-01

Acute myocardial infarction (AMI) is one of the most preventable non-communicable diseases in human. Identifying triggers of myocardial infarction (MI) and prevention ways of exposure-induced complications can reduce morbidity and mortality in people at risk. The aim of this study was to identify the emotional, environmental, physical and chemical dimensions of acute triggers in patients with AMI. This case-crossover study was conducted on 269 patients with AMI, hospitalized at two remedial centers in Rasht in 2015. The study samples were selected by convenient sampling method. Data were collected using researcher-made questionnaire through interviews. Hazard and control periods for each trigger and its effects on the development of MI were studied. The collected data were analyzed using descriptive and analytical statistical methods, Cochran test, and generalized estimating equation (GEE) model with logistics function default in SPSS version 21, and p  < 0.05 was considered statistically significant. The results showed that quarrel ( P  = 0.008, OR = 2.01) and hearing the sudden news ( P  = 0.001, OR = 2.19) were the most common emotional triggers. Respiratory infections ( P  = 0.0001, OR = 6.78) and exposure to hot or cold weather ( P  = 0.005, OR = 2.19) were the most frequent environmental triggers. Doing heavy activities ( P  = 0.005, OR = 1.66) and sexual activities ( P  = 0.003, OR = 2.36) were among the most common physical triggers. High-fat foods consumption and overeating ( P  = 0.0001, OR = 3.79) were the most frequent chemical triggers of AMI. It seems that given the importance of the triggers in the incidence of AMI, planning is necessary to train vulnerable individuals to reduce exposure to triggers.

Climate and environmental triggers of acute myocardial infarction.

PubMed

Claeys, Marc J; Rajagopalan, Sanjay; Nawrot, Tim S; Brook, Robert D

2017-04-01

Over the past few decades, a growing body of epidemiological and clinical evidence has led to heightened concerns about the potential short- and long-term deleterious effects of the environment on cardiovascular health, including the risk for acute myocardial infarction (AMI). This review highlights the increased risk of AMI caused by exposure to air pollution and cold temperatures. These factors should be considered modifiable risk factors in the prevention of cardiovascular disease. The current body of knowledge about the biological mechanisms linking environmental changes to atherothrombotic events and the impact of climate change on cardiovascular health are discussed. Finally, recommendations for prevention and public policy are presented. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.

Effect of initial temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction.

PubMed

Qian, Yuanyu; Liu, Jie; Ma, Jinling; Meng, Qingyi; Peng, Chaoying

2014-07-01

In the present study, the effect of initial body temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction (AMI) patients was investigated. A total of 315 AMI patients were enrolled and the mean temperature was calculated based on their body temperature within 24 h of admission to hospital. The patients were divided into four groups according to their normal body temperature: Group A, <36.5°C; group B, ≥36.5°C and <37.0°C; group C, ≥37.0°C and <37.5°C and group D, ≥37.5°C. The levels of percutaneous coronary intervention, myocardial enzymes and troponin T (TNT), as well as cardiac ultrasound images, were analyzed. Statistically significant differences in the quantity of creatine kinase at 12 and 24 h following admission were identified between group A and groups C and D (P<0.01). A significant difference in TNT at 12 h following admission was observed between groups A and D (P<0.05), however, this difference was not observed with groups B and C. The difference in TNT between the groups at 24 h following admission was not statistically significant (P>0.05). Significant differences in lactate dehydrogenase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed with groups B and C (P>0.05). Significant differences in glutamic-oxaloacetic transaminase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed in groups B and C (P>0.05). However, no significant differences were identified in cardiac function index between all the groups. Therefore, the results of the present study indicated that AMI patients with low initial body temperatures exhibited decreased levels of myocardial enzymes and TNT. Thus, the observation of an initially low body temperature may be used as a protective factor for AMI and may improve the existing clinical program.

Acute kidney injury and cardiovascular outcomes in acute severe hypertension.

PubMed

Szczech, Lynda A; Granger, Christopher B; Dasta, Joseph F; Amin, Alpesh; Peacock, W Frank; McCullough, Peter A; Devlin, John W; Weir, Matthew R; Katz, Jason N; Anderson, Frederick A; Wyman, Allison; Varon, Joseph

2010-05-25

Little is known about the association of kidney dysfunction and outcome in acute severe hypertension. This study aimed to measure the association between baseline chronic kidney disease (estimated glomerular filtration rate), acute kidney injury (AKI, decrease in estimated glomerular filtration rate > or =25% from baseline) and outcome in patients hospitalized with acute severe hypertension. The Studying the Treatment of Acute Hypertension (STAT) registry enrolled patients with acute severe hypertension, defined as > or =1 blood pressure measurement >180 mm Hg systolic and/or >110 mm Hg diastolic and treated with intravenous antihypertensive therapy. Data were compared across groups categorized by admission estimated glomerular filtration rate and AKI during admission. On admission, 79% of the cohort (n=1566) had at least mild chronic kidney disease (estimated glomerular filtration rate <60 mL/min in 46%, <30 mL/min in 22%). Chronic kidney disease patients were more likely to develop heart failure (P<0.0001), non-ST-elevation myocardial infarction (P=0.003), and AKI (P<0.007). AKI patients were at greater risk of heart failure and cardiac arrest (P< or =0.0001 for both). Subjects with AKI experienced higher mortality at 90 days (P=0.003). Any acute loss of estimated glomerular filtration rate during hospitalization was independently associated with an increased risk of death (odds ratio, 1.05; P=0.03 per 10-mL/min decline). Other independent predictors of mortality included increasing age (P<0.0001), male gender (P=0.016), white versus black race (P=0.003), and worse baseline kidney function (P=0.003). Chronic kidney disease is a common comorbidity among patients admitted with acute severe hypertension, and AKI is a frequent form of acute target organ dysfunction, particularly in those with baseline chronic kidney disease. Any degree of AKI is associated with a greater risk of morbidity and mortality.

Rapidly rule out acute myocardial infarction by combining copeptin and heart-type fatty acid-binding protein with cardiac troponin.

PubMed

Jacobs, Leo H J; van Borren, Marcel; Gemen, Eugenie; van Eck, Martijn; van Son, Bas; Glatz, Jan F C; Daniels, Marcel; Kusters, Ron

2015-09-01

The rapid exclusion of acute myocardial infarction in patients with chest pain can reduce the length of hospital admission, prevent unnecessary diagnostic work-up and reduce the burden on our health-care systems. The combined use of biomarkers that are associated with different pathophysiological aspects of acute myocardial infarction could improve the early diagnostic assessment of patients presenting with chest pain. We measured cardiac troponin I, copeptin and heart-type fatty acid-binding protein concentrations in 584 patients who presented to the emergency department with acute chest pain. The diagnostic performances for the diagnosis of acute myocardial infarction and NSTEMI were calculated for the individual markers and their combinations. Separate calculations were made for patients presenting to the emergency department <3 h, 3-6 h and 6-12 h after chest pain onset. For ruling out acute myocardial infarction, the net predictive values (95% CI) of cardiac troponin I, copeptin and heart-type fatty acid-binding protein were 90.4% (87.3-92.9), 84% (79.8-87.6) and 87% (83.5-90), respectively. Combining the three biomarkers resulted in a net predictive value of 95.8% (92.8-97.8). The improvement was most pronounced in the early presenters (<3 h) where the combined net predictive value was 92.9% (87.3-96.5) compared to 84.6% (79.4-88.9) for cardiac troponin I alone. The area under the receiver operating characteristic for the triple biomarker combination increased significantly (P < 0.05) compared to that of cardiac troponin I alone (0.880 [0.833-0.928] vs. 0.840 [0.781-0.898], respectively). Combining copeptin, heart-type fatty acid-binding protein and cardiac troponin I measurements improves the diagnostic performance in patients presenting with chest pain. Importantly, in patients who present early (<3 h) after chest pain onset, the combination improves the diagnostic performance compared to the standard cardiac troponin I measurement alone. �

Wives of patients with acute myocardial infarction are at an increased risk of developing coronary artery disease.

PubMed

Papamichael, Ch; Zampelas, A; Cimponerio, A; Adamopoulos, P N

2002-02-01

The present study was carried out to investigate risk factors for developing coronary artery disease in wives of patients with acute myocardial infarction. Risk factors for developing coronary artery disease were investigated in 50 wives of patients who developed an acute myocardial infarction (group A) and were compared with those of 50 wives of normal healthy men (group B). The average age was 50.20 +/- 1.56 years (mean +/- SD) and 50.20 +/- 1.53 years for group A and group B respectively. The parameters assessed were: plasma cholesterol (TC), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), systolic and diastolic blood pressure, smoking habits and body mass index (BMI). The levels of LDL-C in the wives of patients with myocardial infarction were higher than those of the wives of normal healthy men (167.8 +/- 5.84 mg/dl and 148.4 +/- 4.85 mg/dl, respectively, P < 0.01). Moreover, HDL-C concentrations were lower in the wives of the patients (51.34 +/- 0.92 mg/dl) than in the wives of the healthy men (58.14 +/- 1.39 mg/dl), (P < 0.001). Finally, TG levels were higher in the wives of the patients (132.2 +/- 7.9 mg/dl) than in the wives of the normal healthy men (96.9 +/- 5.94 mg/dl) (P < 0.01). Although plasma lipid levels themselves were not excessively high, the wives of patients with an acute myocardial infarction are at a higher risk of developing coronary artery disease than the wives of normal healthy men, in the long term, due to higher levels of LDL-C and TG as well as lower levels of HDL-C.

Myocardial Extracellular Volume Estimation by CMR Predicts Functional Recovery Following Acute MI.

PubMed

Kidambi, Ananth; Motwani, Manish; Uddin, Akhlaque; Ripley, David P; McDiarmid, Adam K; Swoboda, Peter P; Broadbent, David A; Musa, Tarique Al; Erhayiem, Bara; Leader, Joshua; Croisille, Pierre; Clarysse, Patrick; Greenwood, John P; Plein, Sven

2017-09-01

In the setting of reperfused acute myocardial infarction (AMI), the authors sought to compare prediction of contractile recovery by infarct extracellular volume (ECV), as measured by T1-mapping cardiac magnetic resonance (CMR), with late gadolinium enhancement (LGE) transmural extent. The transmural extent of myocardial infarction as assessed by LGE CMR is a strong predictor of functional recovery, but accuracy of the technique may be reduced in AMI. ECV mapping by CMR can provide a continuous measure associated with the severity of tissue damage within infarcted myocardium. Thirty-nine patients underwent acute (day 2) and convalescent (3 months) CMR scans following AMI. Cine imaging, tissue tagging, T2-weighted imaging, modified Look-Locker inversion T1 mapping natively and 15 min post-gadolinium-contrast administration, and LGE imaging were performed. The ability of acute infarct ECV and acute transmural extent of LGE to predict convalescent wall motion, ejection fraction (EF), and strain were compared per-segment and per-patient. Per-segment, acute ECV and LGE transmural extent were associated with convalescent wall motion score (p < 0.01; p < 0.01, respectively). ECV had higher accuracy than LGE extent to predict improved wall motion (area under receiver-operating characteristics curve 0.77 vs. 0.66; p = 0.02). Infarct ECV ≤0.5 had sensitivity 81% and specificity 65% for prediction of improvement in segmental function; LGE transmural extent ≤0.5 had sensitivity 61% and specificity 71%. Per-patient, ECV and LGE correlated with convalescent wall motion score (r = 0.45; p < 0.01; r = 0.41; p = 0.02, respectively) and convalescent EF (p < 0.01; p = 0.04). ECV and LGE extent were not significantly correlated (r = 0.34; p = 0.07). In multivariable linear regression analysis, acute infarct ECV was independently associated with convalescent infarct strain and EF (p = 0.03; p = 0.04), whereas LGE was not (p = 0.29; p = 0.24). Acute infarct ECV

[Multicenter evaluation of h-FABP semi-quantitative assay (Cardio Detect) in central laboratory: the point in acute myocardial infarction diagnosis].

PubMed

Lefèvre, G; Fayet, J-M; Graïne, H; Berny, C; Maupas-Schwalm, F; Capolaghi, B; Morin, C

2007-01-01

The diagnostic performance of heart-Fatty Acid Binding Protein (h-FABP) (semi-quantitative CardioDetect test) and cardiac troponin I (TnIc) blood assays were compared in one hundred patients presenting with suspicion of acute coronary syndrome. Final patient diagnosis was "acute myocardial infarction" in 36 cases, "non ST myocardial infarction" in 25 cases and "non ischemic pathologies" in 39 cases. h-FABP results were positive in 26 patients, negative in 57 patients and ambiguous in 17 patients, the latter corresponding to the final diagnosis of "acute myocardial infarction" in 5 cases, "non ST myocardial infarction" in 2 cases and "non ischemic pathologies " in 10 cases. At admission, h-FABP and TnIc exhibiteda sensitivity of 54% an 66%, respectively and a specificity of 86% and 95%, respectively. Positive and negative predictive values were 81% and 64% for h-FABP, respectively and 92% and 75% for cTnI, respectively. h-FABP and cTnI demonstrated a similar diagnostic efficiency if admission delay is less than 4 hours after onset of chest pain (area under ROC curve TnIc = 0.767 +/- 0.091 ; area under ROC curve h-FABP = 0.622 +/- 0.109 ; p = 0.144). On the contrary, cTnI assay demonstrated a better efficiency than h-FABP (p< 0.005) for patients admitted in a delay of 4 to 12 hours after the onset of chest pain. If chosen cTnI cut-off corresponded to the recent consensus definition used for monitoring acute coronary syndrome patients, h-FABP semi-quantitative assay realized within central laboratory did not demonstrated a better diagnostic efficiency than cTnI.

Puerarin attenuates severe burn-induced acute myocardial injury in rats.

PubMed

Liu, Sheng; Ren, Hong-Bo; Chen, Xu-Lin; Wang, Fei; Wang, Ren-Su; Zhou, Bo; Wang, Chao; Sun, Ye-Xiang; Wang, Yong-Jie

2015-12-01

Puerarin, the main isoflavone glycoside extracted from the root of Pueraria lobata, is widely prescribed for patients with cardiovascular disorders in China. This study investigates the effect of puerarin on severe burn-induced acute myocardial injury in rats and its underlying mechanisms. Healthy adult Wistar rats were divided into three groups: (1) sham group, sham burn treatment; (2) burn group, third-degree burns over 30% of the total body surface area (TBSA) with lactated Ringer's solution for resuscitation; and (3) burn plus puerarin group, third-degree burns over 30% of TBSA with lactated Ringer's solution containing puerarin for resuscitation. The burned animals were sacrificed at 1, 3, 6, 12, and 24 h after burn injury. Myocardial injury was evaluated by analyzing serum creatine kinase MB fraction (CK-MB) activity and cardiac troponin T (cTNT) level. Changes in cardiomyocyte ultrastructure were also determined using a transmission electron microscope. Tumor necrosis factor (TNF)-α concentration in serum was measured by radioimmunoassay. Cardiac myeloperoxidase (MPO) activity and malondialdehyde (MDA) concentration were measured to determine neutrophil infiltration and oxidative stress in the heart, respectively. The expression of p38 mitogen-activated protein (MAP) kinase in the heart was determined by Western blot analysis. After the 30% TBSA full-thickness burn injury, serum CK-MB activities and cTnT levels increased markedly, both of which were significantly decreased by the puerarin treatment. The level of serum TNF-α concentration in burn group at each time-point was obviously higher than those in sham group (1.09±0.09 ng/ml), and it reached the peak value at 12 h post burn. Burn trauma also resulted in worsen ultrastructural condition, elevated MPO activity and MDA content in heart tissue, and a significant activation of cardiac p38 MAP kinase. Administration of puerarin improved the ultrastructural changes in cardiomyocytes, decreased TNF

Obesity-Induced Endoplasmic Reticulum Stress Causes Lung Endothelial Dysfunction and Promotes Acute Lung Injury.

PubMed

Shah, Dilip; Romero, Freddy; Guo, Zhi; Sun, Jianxin; Li, Jonathan; Kallen, Caleb B; Naik, Ulhas P; Summer, Ross

2017-08-01

Obesity is a significant risk factor for acute respiratory distress syndrome. The mechanisms underlying this association are unknown. We recently showed that diet-induced obese mice exhibit pulmonary vascular endothelial dysfunction, which is associated with enhanced susceptibility to LPS-induced acute lung injury. Here, we demonstrate that lung endothelial dysfunction in diet-induced obese mice coincides with increased endoplasmic reticulum (ER) stress. Specifically, we observed enhanced expression of the major sensors of misfolded proteins, including protein kinase R-like ER kinase, inositol-requiring enzyme α, and activating transcription factor 6, in whole lung and in primary lung endothelial cells isolated from diet-induced obese mice. Furthermore, we found that primary lung endothelial cells exposed to serum from obese mice, or to saturated fatty acids that mimic obese serum, resulted in enhanced expression of markers of ER stress and the induction of other biological responses that typify the lung endothelium of diet-induced obese mice, including an increase in expression of endothelial adhesion molecules and a decrease in expression of endothelial cell-cell junctional proteins. Similar changes were observed in lung endothelial cells and in whole-lung tissue after exposure to tunicamycin, a compound that causes ER stress by blocking N-linked glycosylation, indicating that ER stress causes endothelial dysfunction in the lung. Treatment with 4-phenylbutyric acid, a chemical protein chaperone that reduces ER stress, restored vascular endothelial cell expression of adhesion molecules and protected against LPS-induced acute lung injury in diet-induced obese mice. Our work indicates that fatty acids in obese serum induce ER stress in the pulmonary endothelium, leading to pulmonary endothelial cell dysfunction. Our work suggests that reducing protein load in the ER of pulmonary endothelial cells might protect against acute respiratory distress syndrome in obese

Investigation of ischemia modified albumin, oxidant and antioxidant markers in acute myocardial infarction

PubMed Central

Hazini, Ahmet; Işıldak, İbrahim; Alpdağtaş, Saadet; Önül, Abdullah; Şenel, Ünal; Kocaman, Tuba; Dur, Ali; Iraz, Mustafa; Uyarel, Hüseyin

2015-01-01

Introduction Acute myocardial infarction (AMI) is still one of the most common causes of death worldwide. In recent years, for diagnosis of myocardial ischemia, a new parameter, called ischemia modified albumin (IMA), which is thought to be more advantageous than common methods, has been researched. Aim In this study, systematic analysis of parameters considered to be related to myocardial ischemia has been performed, comparing between control and myocardial ischemia groups. Material and methods We selected 40 patients with AMI and 25 healthy controls for this study. Ischemia modified albumin levels, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) antioxidant enzyme activities and non-enzymatic antioxidants such as retinol, α-tocopherol, β-carotene and ascorbic acid levels were investigated in both groups. Glutathione (GSH) and malondialdehyde (MDA) levels, which are indicators of oxidative stress, were compared between patient and control groups. Results Ischemia modified albumin levels were found significantly higher in the AMI diagnosed group when compared with controls. The MDA level was elevated in the patient group, whereas the GSH level was decreased. SOD, GPx and CAT enzyme levels were decreased in the patient group, where it could be presumed that oxidative stress causes the cardiovascular diseases. Conclusions Due to the increased oxidative stress, non-enzymatic and enzymatic antioxidant capacity was affected. Systematic investigation of parameters related to myocardial infarction has been performed, and it is believed that such parameters can contribute to protection and early diagnosis of AMI and understanding the mechanism of development of the disease. PMID:26677379

When heart goes “BOOM” to fast. Heart rate greater than 80 as mortality predictor in acute myocardial infarction

PubMed Central

Davidovic, Goran; Iric-Cupic, Violeta; Milanov, Srdjan; Dimitijevic, Aleksandra; Petrovic-Janicijevic, Mirjana

2013-01-01

Many prospective studies established association between high heart rate and increased cardiovascular morbidity and mortality, independently of other risk factors. Heart rate over 80 beats per minute more often leads to atherosclerotic plaque disruption, the main step in developing acute coronary syndrome. Purpose was to investigate the incidence of higher heart rate levels in patients with anterior wall acute myocardial infarction with ST-segment elevation and the influence of heart rate on mortality. Research included 140 patients with anterior wall acute myocardial infarction with ST-segment elevation treated in Coronary Unit, Clinical Center Kragujevac in the period from January 2001-June 2006. Heart rate was calculated as the mean value of baseline and heart rate in the first 30 minutes after admission. Other risk factors were also followed to determine their connection with elevated heart rate. Results showed that the majority of patients survived (over 70%). In a total number of patients, more than 75% had a heart rate levels greater than 80 beats per minute. There was a significant difference in heart rate on addmision between survivors and patients who died, with a greater levels in patients with fatal outcome. Both, univariate and multivariate regression analysis singled out heart rate greater than 80 beats per minute as independent mortality predictor in these patients. Heart rate greater than 80 beats per minute is a major, independent risk factor for morbidity and important predictor of mortality in patients with acute myocardial infarction. PMID:23991346

The importance of systematic inquiry in nursing research: An example; women and recovery from acute myocardial infarction.

PubMed

Hamilton, G A

1991-01-01

A review of the literature related to recovery from acute myocardial after discharge from the hospital revealed that very little is known about the recovery period in women. The recovery period has been studied in men with the major focus on cardiac rehabilitation, return to work, and sexual activity. In this descriptive exploratory study women were compared to men in these three areas of recovery within 3 to 9 months after discharge from the hospital. There were statistically significant differences in the following areas: marital status, more women were widowed or single; women had more responsibility for household duties after acute myocardial infarction, a decrease in frequency of sexual activity, and more reports of chest pain during sexual activity. Subjects reported little or no counselling by nurses with regard to cardiac rehabilitation, return to work or household duties, and resumption of sexual activity.

Comparison of primary coronary percutaneous coronary intervention between Diabetic Men and Women with acute myocardial infarction.

PubMed

Liu, Heng-Liang; Liu, Yang; Hao, Zhen-Xuan; Geng, Guo-Ying; Zhang, Zhi-Fang; Jing, Song-Bin; Ba, Ning; Guo, Wei

2015-01-01

This study aimed to explore the short-term efficacy and safety of primary percutaneous coronary intervention (PCI) in female diabetic patients complicated with acute myocardial infarction (AMI). A total of 169 diabetic patients with AMI who underwent primary PCI were selected and divided into group A (52 females) and group B (117 males). The clinical data, characteristics of coronary artery lesions, lengths of hospital stay, and incidences of complications were then compared between two groups. The average age, history of hyperlipidemia, double branch lesions, triple branch lesions, and left main lesions were significantly higher in group A than in group B (P < 0.05). Smoking history, PCI history, and pre-infarction angina were distinctly lower in group A than in group B (P < 0.05). Thrombolysis in myocardial infarction 3 (TIMI3) flow and TIMI myocardial perfusion grade 3 (TMPG3) after PCI were markedly lower in group A than in group B (P < 0.001). Group A had a higher incidence of complications, such as severe arrhythmia, cardiac function Killip III/IV, cardiogenic shock, major, moderate and mild bleed event, as well as a 30-day mortality rate, compared with group B (P < 0.05). In summary, our study demonstrated that female diabetic patients with AMI had lower TIMI3 flow and TMPG3 following PCI than male patients, while there was higher incidence of complications and 30-day mortality rate. Therefore, more attention should be paid to the therapy of diabetic women with acute myocardial infarction as well as the control of risk factors.

Protective effect of active perfusion in porcine models of acute myocardial ischemia

PubMed Central

Feng, Zanxiang; Mao, Zhifu; Dong, Shengjun; Liu, Baohui

2016-01-01

Mortality rates associated with off-pump coronary artery bypass (CAB) are relatively high, as the majority of patients requiring CAB are at a high risk for cardiac events. The present study aimed to establish porcine models of acute myocardial ischemia, and evaluate the protective role of shunt and active perfusion. A total of 30 pigs were randomly assigned to five groups, as follows: i) Sham (control); ii) A1 (shunt; stenosis rate, 55%); iii) A2 (shunt; stenosis rate, 75%); iv) B1 (active perfusion; stenosis rate, 55%); and v) B2 (active perfusion; stenosis rate, 75%) groups. Aortic pressure (P0), left anterior descending coronary pressure (P1), and coronary effective perfusion pressure (P1/P0) were measured. The expression levels of tumor necrosis factor-α (TNF-α), cardiac troponin (cTnI), creatine kinase-myocardial band (CK-MB), interleukin (IL)-6, IL-10, B-cell lymphoma 2 (Bcl-2), and caspase-3 were detected using enzyme-linked immunosorbent assay or western blotting. The myocardial apoptosis rate was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Ischemia models with stenosis rates of 55 and 75% were successfully constructed following suturing of the descending artery. Compared with the control, the 55 and 75% stenosis groups demonstrated significantly decreased P1/P0, increased expression levels of TNF-α, cTnI, CK-MB, IL-6, IL-10 and caspase-3, an increased rate of myocardial apoptosis, and a decreased expression level of anti-apoptotic protein, Bcl-2. At 30 min following successful establishment of the model (ST segment elevation to 1 mm), group B demonstrated significantly increased P1/P0, decreased expression levels of TNF-α, cTnI, CK-MB, IL-6, IL-10 and caspase-3, a decreased rate of myocardial apoptosis, and an increased expression level of anti-apoptotic protein, Bcl-2. Furthermore, the current study indicated that active perfusion was more efficacious in maintaining myocardial perfusion and alleviating

[Papillary muscle rupture complicating acute myocardial infarction--treatment with mitral valve replacement and coronary bypass surgery in acute phase].

PubMed

Kyo, S; Miyamoto, N; Yokote, Y; Ueda, K; Takamoto, S; Omoto, R

1996-06-01

Complete rupture of a papillary muscle following acute myocardial infarction is a severe complication that is typically associated with acute left ventricular failure, pulmonary edema, and relentless clinical deterioration. The reported mortality rates without surgical intervention is almost 90%, therefore, prompt operation without prolonged attempts at medical stabilization is the key to decrease operative mortality. Although the complete coronary revascularization in conjunction with mitral valve replacement is advocated in the western medical academic society, there is only a few case of conjunct surgery has been reported in Japan. Three successful cases of conjunct surgery of mitral valve replacement and coronary complete revascularization in acute phase within one week from the onset of acute myocardial infarction (AMI) are described. There were one male and two female patients with an average age of 60-year-old (range 48-67), who developed cardiogenic shock and admitted to our hospital. The average interval between onset of AMI and the appearance of mitral regurgitation (MR) was 38 hours, and that of the appearance of MR and admission was 40 hours. Surgeries were performed within 26 hours (average 13 hours) after admission. The mitral valve was replaced with a mechanical valve (St. Jude Medical Valve) and a complete coronary revasculatization was done using saphenous vein graft. The average period of operation time and aortic cross clamping time were 6 hours 22 minutes and 109 minutes respectively. The average number of coronary grafting was 2.3 (range 1-3). Postoperative recovery from cardiogenic shock was uneventful in all three patients. The average periods of ICU stay and hospital stay were 5 days and 43 days respectively. All patients have regained their social activities with mean follow up period of 52 months. Since ischemic heart disease remains the leading cause of death in such patients, it is suggested that complete coronary revascularization

Thymol, a dietary monoterpene phenol abrogates mitochondrial dysfunction in β-adrenergic agonist induced myocardial infarcted rats by inhibiting oxidative stress.

PubMed

Nagoor Meeran, M F; Jagadeesh, G S; Selvaraj, P

2016-01-25

Mitochondrial dysfunction has been suggested to be one of the important pathological events in isoproterenol (ISO), a synthetic catecholamine and β-adrenergic agonist induced myocardial infarction (MI). In this context, we have evaluated the impact of thymol against ISO induced oxidative stress and calcium uniporter malfunction involved in the pathology of mitochondrial dysfunction in rats. Male albino Wistar rats were pre and co-treated with thymol (7.5 mg/kg body weight) daily for 7 days. Isoproterenol (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce MI. To explore the extent of cardiac mitochondrial damage, the activities/levels of cardiac marker enzymes, mitochondrial lipid peroxidation products, antioxidants, lipids, calcium, adenosine triphosphate and multi marker enzymes were evaluated. Isoproterenol induced myocardial infarcted rats showed a significant increase in the activities of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, lipids, calcium, and a significant decrease in the activities/levels of heart mitochondrial superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, isocitrate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase, and adenosine triphosphate. Thymol pre and co-treatment showed near normalized effects on all the biochemical parameters studied. Transmission electron microscopic findings and mitochondrial swelling studies confirmed our biochemical findings. The in vitro study also revealed the potent free-radical scavenging activity of thymol. Thus, thymol attenuates the involvement of ISO against oxidative stress and calcium uniporter malfunction associated with mitochondrial dysfunction in rats. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Chronic plus binge ethanol feeding induces myocardial oxidative stress, mitochondrial and cardiovascular dysfunction, and steatosis

PubMed Central

Matyas, Csaba; Varga, Zoltan V.; Mukhopadhyay, Partha; Paloczi, Janos; Lajtos, Tamas; Erdelyi, Katalin; Nemeth, Balazs T.; Nan, Mintong; Hasko, Gyorgy; Gao, Bin

2016-01-01

Alcoholic cardiomyopathy in humans develops in response to chronic excessive alcohol consumption; however, good models of alcohol-induced cardiomyopathy in mice are lacking. Herein we describe mouse models of alcoholic cardiomyopathies induced by chronic and binge ethanol (EtOH) feeding and characterize detailed hemodynamic alterations, mitochondrial function, and redox signaling in these models. Mice were fed a liquid diet containing 5% EtOH for 10, 20, and 40 days (d) combined with single or multiple EtOH binges (5 g/kg body wt). Isocalorically pair-fed mice served as controls. Left ventricular (LV) function and morphology were assessed by invasive pressure-volume conductance approach and by echocardiography. Mitochondrial complex (I, II, IV) activities, 3-nitrotyrosine (3-NT) levels, gene expression of markers of oxidative stress (gp91phox, p47phox), mitochondrial biogenesis (PGC1α, peroxisome proliferator-activated receptor α), and fibrosis were examined. Cardiac steatosis and fibrosis were investigated by histological/immunohistochemical methods. Chronic and binge EtOH feeding (already in 10 days EtOH plus single binge group) was characterized by contractile dysfunction (decreased slope of end-systolic pressure-volume relationship and preload recruitable stroke work), impaired relaxation (decreased time constant of LV pressure decay and maximal slope of systolic pressure decrement), and vascular dysfunction (impaired arterial elastance and lower total peripheral resistance). This was accompanied by enhanced myocardial oxidative/nitrative stress (3-NT; gp91phox; p47phox; angiotensin II receptor, type 1a) and deterioration of mitochondrial complex I, II, IV activities and mitochondrial biogenesis, excessive cardiac steatosis, and higher mortality. Collectively, chronic plus binge EtOH feeding in mice leads to alcohol-induced cardiomyopathies (National Institute on Alcohol Abuse and Alcoholism models) characterized by increased myocardial oxidative

Chronic plus binge ethanol feeding induces myocardial oxidative stress, mitochondrial and cardiovascular dysfunction, and steatosis.

PubMed

Matyas, Csaba; Varga, Zoltan V; Mukhopadhyay, Partha; Paloczi, Janos; Lajtos, Tamas; Erdelyi, Katalin; Nemeth, Balazs T; Nan, Mintong; Hasko, Gyorgy; Gao, Bin; Pacher, Pal

2016-06-01

Alcoholic cardiomyopathy in humans develops in response to chronic excessive alcohol consumption; however, good models of alcohol-induced cardiomyopathy in mice are lacking. Herein we describe mouse models of alcoholic cardiomyopathies induced by chronic and binge ethanol (EtOH) feeding and characterize detailed hemodynamic alterations, mitochondrial function, and redox signaling in these models. Mice were fed a liquid diet containing 5% EtOH for 10, 20, and 40 days (d) combined with single or multiple EtOH binges (5 g/kg body wt). Isocalorically pair-fed mice served as controls. Left ventricular (LV) function and morphology were assessed by invasive pressure-volume conductance approach and by echocardiography. Mitochondrial complex (I, II, IV) activities, 3-nitrotyrosine (3-NT) levels, gene expression of markers of oxidative stress (gp91phox, p47phox), mitochondrial biogenesis (PGC1α, peroxisome proliferator-activated receptor α), and fibrosis were examined. Cardiac steatosis and fibrosis were investigated by histological/immunohistochemical methods. Chronic and binge EtOH feeding (already in 10 days EtOH plus single binge group) was characterized by contractile dysfunction (decreased slope of end-systolic pressure-volume relationship and preload recruitable stroke work), impaired relaxation (decreased time constant of LV pressure decay and maximal slope of systolic pressure decrement), and vascular dysfunction (impaired arterial elastance and lower total peripheral resistance). This was accompanied by enhanced myocardial oxidative/nitrative stress (3-NT; gp91phox; p47phox; angiotensin II receptor, type 1a) and deterioration of mitochondrial complex I, II, IV activities and mitochondrial biogenesis, excessive cardiac steatosis, and higher mortality. Collectively, chronic plus binge EtOH feeding in mice leads to alcohol-induced cardiomyopathies (National Institute on Alcohol Abuse and Alcoholism models) characterized by increased myocardial oxidative

Antimyosin imaging in acute transmural myocardial infarctions: results of a multicenter clinical trial.

PubMed

Johnson, L L; Seldin, D W; Becker, L C; LaFrance, N D; Liberman, H A; James, C; Mattis, J A; Dean, R T; Brown, J; Reiter, A

1989-01-01

Murine monoclonal antimyosin antibody has been shown experimentally to bind selectively to irreversibly damaged myocytes. To evaluate the safety and efficacy of monoclonal antimyosin for identifying acute transmural infarction, 50 patients with acute Q wave myocardial infarction were entered into a phase I/II multicenter trial involving three clinical sites. Indium-111 antimyosin was prepared from an instant kit formulation containing 0.5 mg of diethylene triamine pentaacetic acid (DTPA)-coupled Fab fragment (R11D10) and 1.2 to 2.4 mCi of indium-111. Average labeling efficiency was 92%. Antimyosin was injected 27 +/- 16 h after the onset of chest pain. Planar or tomographic imaging was performed 27 +/- 9 h after injection in all patients, and repeat imaging was done 24 h later in 39 patients. Of the 50 patients entered, 46 showed myocardial uptake of antimyosin (sensitivity 92%). Thirty-one of 39 planar scans performed at 24 h were diagnostic; 8 showed persistent blood pool activity that cleared by 48 h. Focal myocardial uptake of antimyosin corresponded to electrocardiographic infarct localization. No patient had an adverse reaction to antimyosin. In addition, 125 serum samples, including 21 collected greater than 42 days after injection, were tested for human antimouse antibodies, and all samples were assessed as having undetectable titers. Intensity of antimyosin uptake was correlated with infarct location and the presence or absence of collateral vessels. There was a significant correlation between faint uptake and inferoposterior infarct location. In 21 patients who had coronary angiography close to the time of antimyosin injection, there was a significant correlation between faint tracer uptake and closed infarct-related vessel with absent collateral flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute gouty arthritis complicated with acute ST elevation myocardial infarction is independently associated with short- and long-term adverse non-fatal cardiac events.

PubMed

Liu, Kuan-Liang; Lee, Hsin-Fu; Chou, Shing-Hsien; Lin, Yen-Chen; Lin, Chia-Pin; Wang, Chun-Li; Chang, Chi-Jen; Hsu, Lung-An

2014-01-01

Large epidemiologic studies have associated gouty arthritis with the risk of coronary heart disease. However, there has been a lack of information regarding the outcomes for patients who have gout attacks during hospitalization for acute myocardial infarction. We reviewed the data of 444 consecutive patients who were admitted to our hospital between 2005 and 2008 due to acute ST elevation myocardial infarction (STEMI). The clinical outcomes were compared between patients with gout attack and those without. Of the 444, 48 patients with acute STEMI developed acute gouty arthritis during hospitalization. The multivariate analysis identified prior history of gout and estimated glomerular filtration rate as independent risk factors of gout attack for patients with acute STEMI (odds ratio (OR) 21.02, 95 % CI 2.96-149.26, p = 0.002; OR 0.92, 95 % CI 0.86-0.99, p = 0.035, respectively). The in-hospital mortality and duration of hospital stay did not differ significantly between the gouty group and the non-gouty group (controls). During a mean follow-up of 49 ± 28 months, all-cause mortality and stroke were similar for both groups. Multivariate Cox regression showed that gout attack was independently associated with short- and long-term adverse non-fatal cardiac events (hazard ratio (HR) 1.88, 95 % CI 1.09-3.24, p = 0.024; HR 1.82, 95 % CI 1.09-3.03, p = 0.022, respectively). Gout attack among patients hospitalized due to acute STEMI was independently associated with short-term and long-term rates of adverse non-fatal cardiac events.

The Prognostic Value of the Left Ventricular Ejection Fraction Is Dependent upon the Severity of Mitral Regurgitation in Patients with Acute Myocardial Infarction

PubMed Central

Cho, Jung Sun; Youn, Ho-Joong; Her, Sung-Ho; Park, Maen Won; Kim, Chan Joon; Park, Gyung-Min; Cho, Jae Yeong; Ahn, Youngkeun; Kim, Kye Hun; Park, Jong Chun; Seung, Ki Bae; Cho, Myeong Chan; Kim, Chong Jin; Kim, Young Jo; Han, Kyoo Rok; Kim, Hyo Soo

2015-01-01

The prognostic value of the left ventricle ejection fraction (LVEF) after acute myocardial infarction (AMI) has been questioned even though it is an accurate marker of left ventricle (LV) systolic dysfunction. This study aimed to examine the prognostic impact of LVEF in patients with AMI with or without high-grade mitral regurgitation (MR). A total of 15,097 patients with AMI who received echocardiography were registered in the Korean Acute Myocardial Infarction Registry (KAMIR) between January 2005 and July 2011. Patients with low-grade MR (grades 0-2) and high-grade MR (grades 3-4) were divided into the following two sub-groups according to LVEF: LVEF ≤ 40% (n = 2,422 and 197, respectively) and LVEF > 40% (n = 12,252 and 226, respectively). The primary endpoints were major adverse cardiac events (MACE), cardiac death, and all-cause death during the first year after registration. Independent predictors of mortality in the multivariate analysis in AMI patients with low-grade MR were age ≥ 75 yr, Killip class ≥ III, N-terminal pro-B-type natriuretic peptide > 4,000 pg/mL, high-sensitivity C-reactive protein ≥ 2.59 mg/L, LVEF ≤ 40%, estimated glomerular filtration rate (eGFR), and percutaneous coronary intervention (PCI). However, PCI was an independent predictor in AMI patients with high-grade MR. No differences in primary endpoints between AMI patients with high-grade MR (grades 3-4) and EF ≤ 40% or EF > 40% were noted. MR is a predictor of a poor outcome regardless of ejection fraction. LVEF is an inadequate method to evaluate contractile function of the ischemic heart in the face of significant MR. PMID:26130953

Cost-effectiveness of a new short-stay unit to "rule out" acute myocardial infarction in low risk patients.

PubMed

Gaspoz, J M; Lee, T H; Weinstein, M C; Cook, E F; Goldman, P; Komaroff, A L; Goldman, L

1994-11-01

This study attempted to determine the safety and costs of a new short-stay unit for low risk patients who may be admitted to a hospital to rule out myocardial infarction or ischemia. One strategy to reduce the costs of ruling out acute myocardial infarction in low risk patients is to develop alternatives to coronary care units. The short-term and 6-month clinical outcomes and costs for 592 patients admitted to a short-stay coronary observation unit at Brigham and Women's Hospital with a low (< or = 10%) probability of acute myocardial infarction were compared with those for 924 consecutive comparison patients who were eligible for the same unit but were admitted to other hospital settings or discharged home. Actual costs were calculated using detailed cost-accounting methods that incorporated nursing intensity weights. The rate of major complications, recurrent myocardial infarction or cardiac death during 6 months after the initial presentation of the 592 patients admitted to the coronary observation unit was similar to that of the 924 comparison patients before and after adjustment for clinical factors influencing triage and initial diagnoses (adjusted relative risk 0.86, 95% confidence interval 0.49 to 1.53). Their median total costs (25th, 75th percentile) at 6 months ($1,927; 1,455, 3,650) were significantly lower than for comparison patients admitted to the wards $4,712; 1,868, 11,187), to stepdown or intermediate care units ($4,031; 2,069, 9,169) or to the coronary care unit ($9,201; 3,171, 20,011) but were higher than for comparison patients discharged home from the emergency department ($403; 403,927) before and after the same adjustments (all adjusted p < 0.0001). These data suggest that the coronary observation unit may be a safe and cost-saving alternative to current triage strategies for patients with a low risk of acute myocardial infarction admitted from the emergency department. Its replication in other hospitals should be tested.

Pannus-related prosthetic valve dysfunction. Case report

PubMed Central

MOLDOVAN, MARIA-SÎNZIANA; BEDELEANU, DANIELA; KOVACS, EMESE; CIUMĂRNEAN, LORENA; MOLNAR, ADRIAN

2016-01-01

Pannus-related prosthetic valve dysfunction, a complication of mechanical prosthetic valve replacement, is rare, with a slowly progressive evolution, but it can be acute, severe, requiring surgical reintervention. We present the case of a patient with a mechanical single disc aortic prosthesis, with moderate prosthesis-patient mismatch, minor pannus found on previous ultrasound examinations, who presented to our service with angina pain with a duration of 1 hour, subsequently interpreted as non-ST segment elevation myocardial infarction (NSTEMI) syndrome. Coronarography showed normal epicardial coronary arteries, an ample movement of the prosthetic disc, without evidence of coronary thromboembolism, and Gated Single-Photon Emission Computerized Tomography (SPECT) with Technetium (Tc)-99m detected no perfusion defects. Transthoracic echocardiography (TTE) evidenced a dysfunctional prosthesis due to a subvalvular mass; transesophageal echocardiography (TOE) showed the interference of this mass, with a pannus appearance, with the closure of the prosthetic disc. Under conditions of repeated angina episodes, under anticoagulant treatment, surgery was performed, with the intraoperative confirmation of pannus and its removal. Postoperative evolution was favorable. This case reflects the diagnostic and therapeutic management problems of pannus-related prosthetic valve dysfunction. PMID:27004041

Pannus-related prosthetic valve dysfunction. Case report.

PubMed

Moldovan, Maria-Sînziana; Bedeleanu, Daniela; Kovacs, Emese; Ciumărnean, Lorena; Molnar, Adrian

2016-01-01

Pannus-related prosthetic valve dysfunction, a complication of mechanical prosthetic valve replacement, is rare, with a slowly progressive evolution, but it can be acute, severe, requiring surgical reintervention. We present the case of a patient with a mechanical single disc aortic prosthesis, with moderate prosthesis-patient mismatch, minor pannus found on previous ultrasound examinations, who presented to our service with angina pain with a duration of 1 hour, subsequently interpreted as non-ST segment elevation myocardial infarction (NSTEMI) syndrome. Coronarography showed normal epicardial coronary arteries, an ample movement of the prosthetic disc, without evidence of coronary thromboembolism, and Gated Single-Photon Emission Computerized Tomography (SPECT) with Technetium (Tc)-99m detected no perfusion defects. Transthoracic echocardiography (TTE) evidenced a dysfunctional prosthesis due to a subvalvular mass; transesophageal echocardiography (TOE) showed the interference of this mass, with a pannus appearance, with the closure of the prosthetic disc. Under conditions of repeated angina episodes, under anticoagulant treatment, surgery was performed, with the intraoperative confirmation of pannus and its removal. Postoperative evolution was favorable. This case reflects the diagnostic and therapeutic management problems of pannus-related prosthetic valve dysfunction.

Risk factor assessment of young patients with acute myocardial infarction

PubMed Central

Jamil, Gohar; Jamil, Mujgan; AlKhazraji, Hind; Haque, Amber; Chedid, Fares; Balasubramanian, Manjula; Khairallah, Bahaa; Qureshi, Anwer

2013-01-01

The Middle East represents an attractive area for young individuals to seek employment, where they are exposed to numerous environmental conditions. The pursuit of a better standard of living has driven hundreds to the Middle East over the recent decades. This influx has also resulted in a predisposition to premature coronary artery disease (CAD). The aim of this study was to provide an overview of the risk factors in patients younger than 45 years, presenting with acute myocardial infarction (AMI). Out of the 148 patients analyzed, 137 were males and 11 females. 119 were from South Asia and 29 were Arabs. Their mean age was 36 ± 4.2 years. Smoking was the most prevalent risk factor in both groups at 67.6%. This was followed by hypertension, family history of CAD, hyperlipidemia and Diabetes mellitus. There was no significant difference in the clinical risk factor profile between these two groups. ST elevation myocardial infarction (STEMI) was noted in 67.6%, while 32.4% patients suffered a Non ST elevation myocardial infarction (NSTEMI). 84.5% received coronary stents, 8.8% had lone thrombus aspiration or balloon angioplasty only, while the rest were treated by conservative medical management or referred for coronary artery bypass surgery. Conclusion: There is no significant difference in the CAD risk profile between young South Asian and Arab patients. Preventive strategies focused on risk factor reduction, especially smoking cessation, should be implemented to protect young adults in the most productive years of their life. PMID:23991352

Triggering of acute myocardial infarction by different means of transportation.

PubMed

Peters, Annette; von Klot, Stephanie; Mittleman, Murray A; Meisinger, Christine; Hörmann, Allmut; Kuch, Bernhard; Wichmann, H Erich

2013-10-01

Prior studies have reported an association between traffic-related air pollution in urban areas and exacerbation of cardiovascular disease. We assess here whether time spent in different modes of transportation can trigger the onset of acute myocardial infarction (AMI). We performed a case-crossover study. We interviewed consecutive cases of AMI in the KORA Myocardial Infarction Registry in Augsburg, Southern Germany between February 1999 and December 2003 eliciting data on potential triggers in the four days preceding myocardial infarction onset. A total of 1459 cases with known date and time of AMI symptom onset, who had survived 24 hours after the onset, completed the registry's standard interview on potential triggers of AMI. An association between exposure to traffic and AMI onset 1 hour later was observed (odds ratio: 3.2; 95% confidence interval [CI]: 2.7-3.9, p < 0.001). Using a car was the most common source of traffic exposure; nevertheless, times spent in public transport or on a bicycle were similarly associated with AMI onset 1 hour later. While the highest risk for AMI onset was within 1 hour of exposure to traffic, the elevated risk persisted for up to 6 hours. Women, patients aged 65 years or older, patients not part of the workforce, and those with a history of angina or diabetes exhibited the largest associations between times spent in traffic and AMI onset 1 hour later. The data suggest that transient exposure to traffic regardless of the means of transportation may increase the risk of AMI transiently.

Detection of von Willebrand factor and tissue factor in platelets-fibrin rich coronary thrombi in acute myocardial infarction.

PubMed

Yamashita, Atsushi; Sumi, Takahiro; Goto, Shinya; Hoshiba, Yasunari; Nishihira, Kensaku; Kawamoto, Riichirou; Hatakeyama, Kinta; Date, Haruhiko; Imamura, Takuroh; Ogawa, Hisao; Asada, Yujiro

2006-01-01

The rapid closure of coronary arteries due to occlusive thrombi is the major cause of acute myocardial infarction. However, the mechanisms of coronary thrombus formation have not been elucidated. We immunohistochemically assessed the localizations and their changes over time of glycoprotein IIb/IIIa, fibrin, von Willebrand factor (vWF), and tissue factor (TF), after the onset of chest pain (<4, 4 to 6, or 6 to 12 hours), in fresh coronary thrombi causing acute myocardial infarction. The occlusive thrombi were consistently composed of platelets, fibrin, vWF, and TF from the early phase of onset, and glycoprotein IIb/IIIa and fibrin were closely associated with vWF and TF, respectively. vWF and/or TF may contribute to occlusive thrombus formation and be novel therapeutic candidates for treating patients with coronary thrombosis.

Autonomic responses during acute myocardial infarction in the rat model: implications for arrhythmogenesis.

PubMed

Kolettis, Theofilos M; Kontonika, Marianthi; Lekkas, Panagiotis; Vlahos, Antonios P; Baltogiannis, Giannis G; Gatzoulis, Konstantinos A; Chrousos, George P

2018-04-10

Autonomic responses participate in the pathophysiology of acute myocardial infarction, but their precise time course remains unclear. Here, we investigated the autonomic activity and ventricular tachyarrhythmias in conscious, unrestrained rats post-infarction. The left coronary artery was ligated in 12 Wistar rats, and six rats were sham operated, followed by 24-h electrocardiographic recording via implanted telemetry transmitters. Sympathetic activity was assessed by detrended fluctuation analysis and vagal activity by time- and frequency-domain analysis of heart rate variability. The duration of the ventricular tachyarrhythmias was measured, and voluntary motion served as a marker of heart failure. In sham-operated rats, heart rate and sympathetic activity remained low, whereas vagal activity rose progressively after the fourth hour. Post-ligation, medium-sized antero-septal necrosis was observed, reaching ~20% of the left ventricular volume; tachyarrhythmias were frequent, displaying a bimodal curve, and motion counts were low. Vagal activity decreased early post-ligation, coinciding with a high incidence of tachyarrhythmias, but tended to rise subsequently in rats with higher motion counts. Sympathetic activity increased after the third hour, along with a second tachyarrhythmia peak, and remained elevated throughout the 24-h period. Vagal withdrawal, followed by gradual sympathetic activation, may participate in arrhythmogenesis during acute myocardial infarction.

Effects of intravenous magnesium in suspected acute myocardial infarction: overview of randomised trials.

PubMed Central

Teo, K K; Yusuf, S; Collins, R; Held, P H; Peto, R

1991-01-01

OBJECTIVE--To investigate the effect of intravenous magnesium on mortality in suspected acute myocardial infarction. DESIGN--Systematic overview of all available randomised trials in which patients were allocated to receive either intravenous magnesium or otherwise similar treatment without magnesium. SETTING--Coronary care units of several hospitals. PATIENTS--1301 patients in seven randomised trials. MAIN OUTCOME MEASURE--Short term mortality. RESULTS--Considering the seven trials collectively there were 25 (3.8%) deaths among 657 patients allocated to receive magnesium and 53 (8.2%) deaths among 644 patients allocated control, generally during hospital follow up. This represents a 55% reduction in the odds of death (p less than 0.001) with 95% confidence intervals ranging from about one third to about two thirds. 70 of 648 patients allocated magnesium compared with 109 of 641 controls had serious ventricular arrhythmias, suggesting that magnesium reduces the incidence, though the definition varied among trials. Other adverse effects were rare in the limited number of patients for whom this data were available. CONCLUSION--Despite the limited number of patients randomised this overview suggests that intravenous magnesium therapy may reduce mortality in patients with acute myocardial infarction. Further large scale trials to confirm (or refute) these findings are desirable. PMID:1838289

Non-contrast T1-mapping detects acute myocardial edema with high diagnostic accuracy: a comparison to T2-weighted cardiovascular magnetic resonance

PubMed Central

2012-01-01

Background T2w-CMR is used widely to assess myocardial edema. Quantitative T1-mapping is also sensitive to changes in free water content. We hypothesized that T1-mapping would have a higher diagnostic performance in detecting acute edema than dark-blood and bright-blood T2w-CMR. Methods We investigated 21 controls (55 ± 13 years) and 21 patients (61 ± 10 years) with Takotsubo cardiomyopathy or acute regional myocardial edema without infarction. CMR performed within 7 days included cine, T1-mapping using ShMOLLI, dark-blood T2-STIR, bright-blood ACUT2E and LGE imaging. We analyzed wall motion, myocardial T1 values and T2 signal intensity (SI) ratio relative to both skeletal muscle and remote myocardium. Results All patients had acute cardiac symptoms, increased Troponin I (0.15-36.80 ug/L) and acute wall motion abnormalities but no LGE. T1 was increased in patient segments with abnormal and normal wall motion compared to controls (1113 ± 94 ms, 1029 ± 59 ms and 944 ± 17 ms, respectively; p < 0.001). T2 SI ratio using STIR and ACUT2E was also increased in patient segments with abnormal and normal wall motion compared to controls (all p < 0.02). Receiver operator characteristics analysis showed that T1-mapping had a significantly larger area-under-the-curve (AUC = 0.94) compared to T2-weighted methods, whether the reference ROI was skeletal muscle or remote myocardium (AUC = 0.58-0.89; p < 0.03). A T1 value of greater than 990 ms most optimally differentiated segments affected by edema from normal segments at 1.5 T, with a sensitivity and specificity of 92 %. Conclusions Non-contrast T1-mapping using ShMOLLI is a novel method for objectively detecting myocardial edema with a high diagnostic performance. T1-mapping may serve as a complementary technique to T2-weighted imaging for assessing myocardial edema in ischemic and non-ischemic heart disease, such as quantifying area-at-risk and diagnosing

Serum Chloride and Sodium Interplay in Patients With Acute Myocardial Infarction and Heart Failure With Reduced Ejection Fraction: An Analysis From the High-Risk Myocardial Infarction Database Initiative.

PubMed

Ferreira, João Pedro; Girerd, Nicolas; Duarte, Kevin; Coiro, Stefano; McMurray, John J V; Dargie, Henry J; Pitt, Bertram; Dickstein, Kenneth; Testani, Jeffrey M; Zannad, Faiez; Rossignol, Patrick

2017-02-01

Serum chloride levels were recently found to be independently associated with mortality in heart failure (HF). We investigated the relationship between serum chloride and clinical outcomes in 7195 subjects with acute myocardial infarction complicated by reduced left ventricular function and HF. The studied outcomes were all-cause mortality, cardiovascular mortality, and hospitalization for HF. Both chloride and sodium had a nonlinear association with the studied outcomes (P<0.05 for linearity). Patients in the lowest chloride tertile (chloride ≤100) were older, had more comorbidities, and had lower sodium levels (P<0.05 for all). Serum chloride showed a significant interaction with sodium with regard to all studied outcomes (P for interaction <0.05 for all). The lowest chloride tertile (≤100 mmol/L) was associated with increased mortality rates in the context of lower sodium (≤138 mmol/L; adjusted hazard ratio [95% confidence interval] for all-cause mortality=1.42 (1.14-1.77); P=0.002), whereas in the context of higher sodium levels (>141 mmol/L), the association with mortality was lost. Spline-transformed chloride and its interaction with sodium did not add significant prognostic information on top of other well-established prognostic variables (P>0.05 for all outcomes). In post-myocardial infarction with systolic dysfunction and HF, low serum chloride was associated with mortality (but not hospitalization for HF) in the setting of lower sodium. Overall, chloride and its interaction with sodium did not add clinically relevant prognostic information on top of other well-established prognostic variables. Taken together, these data support an integrated and critical consideration of chloride and sodium interplay. © 2017 American Heart Association, Inc.

Reduced Admissions for Acute Myocardial Infarction Associated with a Public Smoking Ban: Matched Controlled Study

ERIC Educational Resources Information Center

Seo, Dong-Chul; Torabi, Mohammad R.

2007-01-01

There has been no research linking implementation of a public smoking ban and reduced incidence of acute myocardial infarction (AMI) among nonsmoking patients. An ex post facto matched control group study was conducted to determine whether there was a change in hospital admissions for AMI among nonsmoking patients after a public smoking ban was…

Cortistatin Improves Cardiac Function After Acute Myocardial Infarction in Rats by Suppressing Myocardial Apoptosis and Endoplasmic Reticulum Stress.

PubMed

Shi, Zhi-Yu; Liu, Yue; Dong, Li; Zhang, Bo; Zhao, Meng; Liu, Wen-Xiu; Zhang, Xin; Yin, Xin-Hua

2016-04-18

The endoplasmic reticulum (ER) stress-induced apoptotic pathway is associated with the development of acute myocardial infarction (AMI). Cortistatin (CST) is a novel bioactive peptide that inhibits apoptosis-related injury. Therefore, we investigated the cardioprotective effects and potential mechanisms of CST in a rat model of AMI. Male Wistar rats were randomly divided into sham, AMI, and AMI + CST groups. Cardiac function and the degree of infarction were evaluated by echocardiography, cardiac troponin I activity, and 2,3,5-triphenyl-2H-tetrazolium chloride staining after 7 days. The expression of CST, ER stress markers, and apoptotic markers was examined using immunohistochemistry and Western blotting. Compared to the AMI group, the AMI + CST group exhibited markedly better cardiac function and a lower degree of infarction. Electron microscopy and terminal deoxynucleotidyl transferase dUTP nick end labeling confirmed that myocardial apoptosis occurred after AMI. Cortistatin treatment reduced the expression of caspase 3, cleaved caspase 3, and Bax (proapoptotic proteins) and promoted the expression of Bcl-2 (antiapoptotic protein). In addition, the reduced expression of glucose-regulated protein 94 (GRP94), glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding proteins homologous protein, and caspase 12 indicated that ER stress and the apoptotic pathway associated with ER stress were suppressed. Exogenous CST has a notable cardioprotective effect after AMI in a rat model in that it improves cardiac function by suppressing ER stress and myocardial apoptosis. © The Author(s) 2016.

Functional Cardiac Magnetic Resonance Imaging (MRI) in the Assessment of Myocardial Viability and Perfusion

PubMed Central

2003-01-01

Executive Summary Objective The objective of this health technology policy assessment was to determine the effectiveness safety and cost-effectiveness of using functional cardiac magnetic resonance imaging (MRI) for the assessment of myocardial viability and perfusion in patients with coronary artery disease and left ventricular dysfunction. Results Functional MRI has become increasingly investigated as a noninvasive method for assessing myocardial viability and perfusion. Most patients in the published literature have mild to moderate impaired LV function. It is possible that the severity of LV dysfunction may be an important factor that can alter the diagnostic accuracy of imaging techniques. There is some evidence of comparable or better performance of functional cardiac MRI for the assessment of myocardial viability and perfusion compared with other imaging techniques. However limitations to most of the studies included: Functional cardiac MRI studies that assess myocardial viability and perfusion have had small sample sizes. Some studies assessed myocardial viability/perfusion in patients who had already undergone revascularization, or excluded patients with a prior MI (Schwitter et al., 2001). Lack of explicit detail of patient recruitment. Patients with LVEF >35%. Interstudy variability in post MI imaging time(including acute or chronic MI), when patients with a prior MI were included. Poor interobserver agreement (kappa statistic) in the interpretation of the results. Traditionally, 0.80 is considered “good”. Cardiac MRI measurement of myocardial perfusion to as an adjunct tool to help diagnose CAD (prior to a definitive coronary angiography) has also been examined in some studies, with methodological limitations, yielding comparable results. Many studies examining myocardial viability and perfusion report on the accuracy of imaging methods with limited data on long-term patient outcome and management. Kim et al. (2000) revealed that the transmural

Galectin-3: A Link between Myocardial and Arterial Stiffening in Patients with Acute Decompensated Heart Failure?

PubMed

Lala, Radu Ioan; Darabantiu, Dan; Pilat, Luminita; Puschita, Maria

2016-02-01

Heart failure is accompanied by abnormalities in ventricular-vascular interaction due to increased myocardial and arterial stiffness. Galectin-3 is a recently discovered biomarker that plays an important role in myocardial and vascular fibrosis and heart failure progression. The aim of this study was to determine whether galectin-3 is correlated with arterial stiffening markers and impaired ventricular-arterial coupling in decompensated heart failure patients. A total of 79 inpatients with acute decompensated heart failure were evaluated. Serum galectin-3 was determined at baseline, and during admission, transthoracic echocardiography and measurements of vascular indices by Doppler ultrasonography were performed. Elevated pulse wave velocity and low arterial carotid distensibility are associated with heart failure in patients with preserved ejection fraction (p = 0.04, p = 0.009). Pulse wave velocity, carotid distensibility and Young's modulus did not correlate with serum galectin-3 levels. Conversely, raised galectin-3 levels correlated with an increased ventricular-arterial coupling ratio (Ea/Elv) p = 0.047, OR = 1.9, 95% CI (1.0‑3.6). Increased galectin-3 levels were associated with lower rates of left ventricular pressure rise in early systole (dp/dt) (p=0.018) and raised pulmonary artery pressure (p = 0.046). High galectin-3 levels (p = 0.038, HR = 3.07) and arterial pulmonary pressure (p = 0.007, HR = 1.06) were found to be independent risk factors for all-cause mortality and readmissions. This study showed no significant correlation between serum galectin-3 levels and arterial stiffening markers. Instead, high galectin-3 levels predicted impaired ventricular-arterial coupling. Galectin-3 may be predictive of raised pulmonary artery pressures. Elevated galectin-3 levels correlate with severe systolic dysfunction and together with pulmonary hypertension are independent markers of outcome.

Impact of sleep-disordered breathing in patients with acute myocardial infarction: a retrospective analysis.

PubMed

Gessner, Verena; Bitter, Thomas; Horstkotte, Dieter; Oldenburg, Olaf; Fox, Henrik

2017-10-01

Sleep-disordered breathing (SDB) is associated with an increased risk of cardiovascular events. Previous studies showed that severe SDB has a negative impact on myocardial salvage and progression of left ventricular dysfunction after acute myocardial infarction (AMI). This study investigated the frequency of SDB and the effects of SDB on left ventricular function after AMI. This retrospective study enrolled all patients with AMI who had undergone cardiorespiratory polygraphy for SDB diagnosis. The apnea-hypopnea index was used as a standard metric of SDB severity. SDB was classified as mild (apnea-hypopnea index >5 to <15 per h), moderate (≥15 to <30 per h) or severe (apnea-hypopnea index ≥30 per h). According to the majority of events, SDB was classified as predominant obstructive sleep apnea, central sleep apnea or mixed sleep apnea (mixed SDB). A total of 223 patients with AMI (112 with ST elevation and 111 without ST elevation; 63.2 ± 11.2 years, 82% male, left ventricular ejection fraction 49 ± 12%) were enrolled. SDB was present in 85.6%, and was moderate-to-severe in 63.2%; 40.8% had obstructive sleep apnea, 41.7% had central sleep apnea and 3.1% had mixed SDB. Left ventricular ejection fraction was lower in patients with AMI with severe SDB (45 ± 14%) versus those without SDB (57 ± 7%; P < 0.005). In addition, lower left ventricular ejection fraction (≤45%) was associated with increased frequency (apnea-hypopnea index ≥5 per h in 96%) and severity (apnea-hypopnea index ≥30 per h in 48%) of SDB in general and a higher percentage of central sleep apnea (57%) in particular. SDB is highly frequent in patients with AMI. SDB severity appeared to be linked to impaired left ventricular function, especially in patients with central sleep apnea. © 2017 European Sleep Research Society.

Association Between Hyperuricemia and Major Adverse Cardiac Events in Patients with Acute Myocardial Infarction.

PubMed

Ranjith, Naresh; Myeni, Nomcebo N; Sartorius, Ben; Mayise, Chamsanqua

2017-02-01

To investigate the association between hyperuricemia and major adverse cardiac events (MACE) in patients with acute myocardial infarction (AMI). Consecutive patients admitted with AMI to the Coronary Care Unit at R. K. Khan Hospital (Durban, South Africa) between the years 2006 and 2014 were included. Demographic data, including clinical and biochemical information stored in an electronic database, were obtained from all patients. A total of 2683 patients were studied, of whom 65% were males. The mean age of the participants was 57.1 ± 11.5 years, with 79% presenting with ST elevation myocardial infarction. Sixty-one percent were smokers, 59% had diabetes mellitus, 52% had hypertension, and 58% presented with a family history of premature coronary artery disease. Twenty-six percent (n = 690) had hyperuricemia, were older (59 ± 12.1 vs. 56.5 ± 11.2 years) and more likely to present with hypertension (P < 0.001), lower ejection fraction (P < 0.001), and higher median creatinine levels (P < 0.001). A significantly greater proportion of patients with hyperuricemia experienced MACE (45% vs. 30%, P < 0.001). In both sexes, considerable heterogeneity for risk factors and clinical events was noted in individuals with hyperuricemia. Multivariable analyses for risk factors associated with mortality suggest that hyperuricemia conferred a significantly increased risk of mortality after adjustment [odds ratio (OR) 1.7 (95% confidence interval 1.0-2.8); P = 0.042]. A significant increasing risk trend for MACE was observed for increasing tertiles of serum uric acid concentrations above normal (P < 0.001), particularly for cardiac failure (P < 0.001) and death (P = 0.006). Hyperuricemia is significantly associated with hypertension, renal dysfunction, MACE, and independently confers a higher risk of mortality in patients with AMI. Significant heterogeneity was found by gender for risk factors and clinical events in individuals

Cardioprotective effect of sulphonated formononetin on acute myocardial infarction in rats.

PubMed

Zhang, Shumin; Tang, Xuexi; Tian, Jingwei; Li, Chunmei; Zhang, Guanbo; Jiang, Wanglin; Zhang, Zunting

2011-06-01

This study was designed to investigate the therapeutic effect of sodium formononetin-3'-sulphonate (Sul-F), a water-soluble derivate of formononetin, on acute myocardial infarction in rats. The results showed that treatment with Sul-F significantly prevented the elevation of ST-segment level, decreased the contents of creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase and cardiac troponin T in serum and reduced the myocardium necrosis scores. The number of apoptosis cardiocytes is well accordance with the up-regulated expression of Bcl-2 and the down-regulated expression of Bax. Meanwhile, Sul-F significantly increased the cardiac mitochondrial ATP content, improved ATP synthase activity, decreased thiobarbituric acid-reactive substances content and attenuated the decrease in superoxide dismutase and glutathione peroxidase activities. These findings indicate that Sul-F has a protective potential against myocardial infarction injury. A possible mechanism for the protective effect is the elevated expression of endogenous antioxidant defence enzymes degraded lipid peroxidation products and improved energy metholism of cardiac mitochondrial, thus attenuating cardiocyte apoptosis. © 2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.

CD8+CD28+ T cells might mediate injury of cardiomyocytes in acute myocardial infarction.

PubMed

Zhang, Lili; Wang, Zhiyan; Wang, Di; Zhu, Jumo; Wang, Yi

2018-06-07

CD8 + T cells accumulate in the necrotic myocardium of acute myocardial infarction (AMI). It is unclear whether CD8 + CD28 + T cells, a specific subset of CD8 + T cells, contribute to myocardial injury. In this study, 92 consecutive patients with AMI and 28 healthy control subjects were enrolled. The frequency of CD8 + CD28 + T cells in peripheral blood samples was assayed by flow cytometry. Plasma cardiac troponin I (TNI) and left ventricular ejection fraction (LVEF) were determined. Long-term prognosis of the patients was evaluated by major adverse cardiac and cerebrovascular events (MACCE) over a 12-month follow-up period. Our findings indicated that patients with AMI who presented with high numbers of CD8 + CD28 + T cells had an increased infarction size and aggravated ventricular function. We proposed that cytotoxic CD8 + CD28 + T cell-mediated myocardial necrosis may act as a novel and alternative pathway of AMI. Copyright © 2018 Elsevier Ltd. All rights reserved.

A case of acute myocardial infarction due to the use of cayenne pepper pills.

PubMed

Sayin, Muhammet Rasit; Karabag, Turgut; Dogan, Sait Mesut; Akpinar, Ibrahim; Aydin, Mustafa

2012-04-01

The use of weight loss pills containing cayenne pepper has ever been increasing. The main component of cayenne pepper pills is capsaicin. There are conflicting data about the effects of capsaicin on the cardiovascular system. In this paper, we present the case of a 41 year old male patient with no cardiovascular risk factors who took cayenne pepper pills to lose weight and developed acute myocardial infarction.

Incidence, mechanisms, predictors, and clinical impact of acute and late stent malapposition after primary intervention in patients with acute myocardial infarction: an intravascular ultrasound substudy of the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial.

PubMed

Guo, Ning; Maehara, Akiko; Mintz, Gary S; He, Yong; Xu, Kai; Wu, Xiaofan; Lansky, Alexandra J; Witzenbichler, Bernhard; Guagliumi, Giulio; Brodie, Bruce; Kellett, Mirle A; Dressler, Ovidiu; Parise, Helen; Mehran, Roxana; Stone, Gregg W

2010-09-14

The incidence and mechanisms of acute and late stent malapposition after primary stent implantation in ST-segment elevation myocardial infarction remain unclear. The Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial was a dual-arm, factorial, randomized trial comparing paclitaxel-eluting stents (PES) and otherwise equivalent bare metal stents (BMS) in ST-segment elevation myocardial infarction patients. The intravascular ultrasound substudy enrolled 241 patients with 263 native coronary lesions (201 PES, 62 BMS) with baseline and 13-month follow-up imaging. Postintervention acute stent malapposition (ASM) occurred in 34.3% PES- and 40.3% BMS-treated lesions. Of these, 39.1% PES- and 40.0% BMS-treated lesions resolved at follow-up, especially within the stent body (66.7%); complete resolution was accompanied by a reduction in external elastic membrane area. An ASM area >1.2 mm(2) best separated persistent from resolved ASM. At follow-up, a higher frequency of late stent malapposition was detected in PES-treated lesions (46.8%) mainly because of more late acquired stent malapposition (30.8%) compared with BMS-treated lesions. Late acquired stent malapposition area correlated to the decrease of peri-stent plaque in the subset of lesions without positive remodeling and only to change in external elastic membrane in the group with positive remodeling. Independent predictors of late acquired stent malapposition were plaque/thrombus protrusion (odds ratio, 5.60; 95% confidence interval [CI], 2.32 to 13.54) and PES use (odds ratio, 6.32; 95% CI, 2.15 to 18.62). The incidence of ASM was similar in PES- and BMS-treated lesions, but late acquired stent malapposition was more common in PES-treated lesions. The reason for resolved ASM was negative remodeling, with larger ASM areas separating persistent from resolved ASM. Late acquired stent malapposition was due mainly to positive remodeling and plaque/thrombus resolution

Cardiac-Specific Overexpression of Catalase Attenuates Lipopolysaccharide-Induced Myocardial Contractile Dysfunction: Role of Autophagy

PubMed Central

Turdi, Subat; Han, Xuefeng; Huff, Anna F.; Roe, Nathan D.; Hu, Nan; Gao, Feng; Ren, Jun

2012-01-01

Lipopolysaccharide (LPS) from Gram-negative bacteria is a major initiator of sepsis, leading to cardiovascular collapse. Accumulating evidence has indicated a role of reactive oxygen species (ROS) in cardiovascular complication in sepsis. This study was designed to examine the effect of cardiac-specific overexpression of catalase in LPS-induced cardiac contractile dysfunction and the underlying mechanism(s) with a focus on autophagy. Catalase transgenic and wild-type FVB mice were challenged with LPS (6 mg/kg) and cardiac function was evaluated. Levels of oxidative stress, autophagy, apoptosis and protein damage were examined using fluorescence microscopy, Western blot, TUNEL assay, caspase-3 activity and carbonyl formation. Kaplan-Meier curve was constructed for survival following LPS treatment. Our results revealed a lower mortality in catalase mice compared with FVB mice following LPS challenge. LPS injection led to depressed cardiac contractile capacity as evidenced by echocardiography and cardiomyocyte contractile function, the effect of which was ablated by catalase overexpression. LPS treatment induced elevated TNF-α level, autophagy, apoptosis (TUNEL, caspase-3 activation, cleaved caspase-3), production of ROS and O2−, and protein carbonyl formation, the effects of which were significantly attenuated by catalase overexpression. Electron microscopy revealed focal myocardial damage characterized by mitochondrial injury following LPS treatment, which was less severe in catalase mice. Interestingly, LPS-induced cardiomyocyte contractile dysfunction was prevented by antioxidant NAC and the autophagy inhibitor 3-methyladenine. Taken together, our data revealed that catalase protects against LPS-induced cardiac dysfunction and mortality, which may be associated with inhibition of oxidative stress and autophagy. PMID:22902401

Correlation between cardiac remodelling, function, and myocardial contractility in rat hearts 5 weeks after myocardial infarction.

PubMed

Gosselin, H; Qi, X; Rouleau, J L

1998-01-01

Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papillary muscle studies 5 weeks after infarction. Morphologic studies were also done. Rats with large infarctions (54%) had marked ventricular dilatation (dilatation index from 0.23 to 0.75, p < 0.01) and papillary muscle dysfunction (total tension from 6.7 to 3.2 g/mm2, p < 0.01) but only moderate left ventricular dysfunction (maximum developed tension from 206 to 151 mmHg (1 mmHg = 133.3 Pa), p < 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myocardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p < 0.01). Rats with moderate infarctions (32%) had less marked but still moderate ventricular dilatation (dilatation index 0.37, p < 0.001) and moderate papillary muscle dysfunction (total tension 4.2 g/mm2, p < 0.01). However, their decrease in ventricular function was only mild (maximum developed pressure 178 mmHg, p < 0.01) and less than one would expect with an infarct size of 32%. The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns). We conclude that in this postinfarction model, in large myocardial infarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction and that papillary muscle studies slightly

Effect of streptokinase on reperfusion after acute myocardial infarction and its complications: an ex-post facto study.

PubMed

Taheri, Leila; Boroujeni, Ali Zargham; Kargar Jahromi, Marzieh; Charkhandaz, Maryam; Hojat, Mohsen

2015-01-01

Emergency treatment of patients with acute myocardial infarction is very important. Streptokinase in Iran is often as the only clot-busting medication is used. The purpose of using streptokinase medication is to revive the ischemic heart tissue, although has dangerous complications too. Therefore, the present study aimed to determine the effect of streptokinase on reperfusion after acute myocardial infarction and its complications, has been designed and conducted. This is an Ex-post facto study. The study population included patients who suffer from acute myocardial infarction. The sample size was 300 patients, and 2 groups were matched, in variables of age, sex, underlying disease, frequencies and area of MI. Data collection did by researcher making questionnaire, that accept face and content validity by 10 expert researcher, the reliability was conducted with Spearman's test (r=0.85) by Test-retest method. Data analysis did by SPSS software: V 12. Mean of EF in SK group was (46.15±8.11) and in control group was (43.11±12.57). Significant relationship was seen between SK, arrhythmia occurring and improve EF reperfusion by chi-square test (p=0.028), (p=0.020).The most arrhythmia in SK group was Ventricular Tachycardia (20.7%). Significant statistical relation between SK and mortality were found by Chi-square test (p=0.001). But a meaningful statistical relation was not found between SK and pulmonary edema incidence (p=0.071). Nurses of CCU should be aware about SK complications such as hypotension, bleeding and arrhythmias. Proposed compare SK and tissue plasminogen drug in reperfusion and complications effect.

Diagnostic Accuracy of a New Cardiac Electrical Biomarker for Detection of Electrocardiogram Changes Suggestive of Acute Myocardial Ischemic Injury

PubMed Central

Schreck, David M; Fishberg, Robert D

2014-01-01

Objective A new cardiac “electrical” biomarker (CEB) for detection of 12-lead electrocardiogram (ECG) changes indicative of acute myocardial ischemic injury has been identified. Objective was to test CEB diagnostic accuracy. Methods This is a blinded, observational retrospective case-control, noninferiority study. A total of 508 ECGs obtained from archived digital databases were interpreted by cardiologist and emergency physician (EP) blinded reference standards for presence of acute myocardial ischemic injury. CEB was constructed from three ECG cardiac monitoring leads using nonlinear modeling. Comparative active controls included ST voltage changes (J-point, ST area under curve) and a computerized ECG interpretive algorithm (ECGI). Training set of 141 ECGs identified CEB cutoffs by receiver-operating-characteristic (ROC) analysis. Test set of 367 ECGs was analyzed for validation. Poor-quality ECGs were excluded. Sensitivity, specificity, and negative and positive predictive values were calculated with 95% confidence intervals. Adjudication was performed by consensus. Results CEB demonstrated noninferiority to all active controls by hypothesis testing. CEB adjudication demonstrated 85.3–94.4% sensitivity, 92.5–93.0% specificity, 93.8–98.6% negative predictive value, and 74.6–83.5% positive predictive value. CEB was superior against all active controls in EP analysis, and against ST area under curve and ECGI by cardiologist. Conclusion CEB detects acute myocardial ischemic injury with high diagnostic accuracy. CEB is instantly constructed from three ECG leads on the cardiac monitor and displayed instantly allowing immediate cost-effective identification of patients with acute ischemic injury during cardiac rhythm monitoring. PMID:24118724

Velocity vector imaging fails to quantify regional myocardial dysfunction in a mouse model of isoprenaline-induced cardiotoxicity.

PubMed

Täng, Margareta Scharin; Redfors, Bjorn; Shao, Yangzhen; Omerovic, Elmir

2012-08-01

Regional myocardial deformation patterns are important in a variety of cardiac diseases, including stress-induced cardiomyopathy. Velocity-vector-based imaging is a speckle-tracking echocardiography (STE)-based algorithm that has been shown to allow in-depth cardiac phenotyping in humans. Regional posterior wall myocardial dysfunction occurs during severe isoprenaline stress in mice. We have previously shown that regional posterior wall end-systolic transmural strain decreases after severe isoprenaline toxicity in mice. We hypothesize that STE can detect and further quantify these perturbations. Twenty-three mice underwent echocardiographic examination using the VEVO2100 system. Regional transmural radial strain and strain rate were calculated in both parasternal short-axis and parasternal long-axis cine loops using the VisualSonics VEVO 2100 velocity vector imaging (VVI) STE algorithm. Eight C57BL/6 mice underwent baseline echocardiographic examination using the VisualSonics VEVO 770 system, which can acquire >1,000 frames/s cine loops. In a parasternal short-axis cine loop, the heart was divided into six segments, and regional fractional wall thickening (FWT) was assessed manually. The same protocols were also performed 90 minutes post 400 mg/kg intraperitoneally isoprenaline. Regional myocardial FWT is uniform at baseline but increases significantly in anterolateral segments, whereas it decreases significantly in posterior segments (P < 0.05). A similar pattern is seen using the VVI algorithm although the variance is larger, and differences are smaller and fail to reach significance. VVI is less sensitive in detecting regional perturbations in myocardial function than manual tracing, possibly due to the low frame rate in the cine loops used. © 2012, Wiley Periodicals, Inc.

CVIT expert consensus document on primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) in 2018.

PubMed

Ozaki, Yukio; Katagiri, Yuki; Onuma, Yoshinobu; Amano, Tetsuya; Muramatsu, Takashi; Kozuma, Ken; Otsuji, Satoru; Ueno, Takafumi; Shiode, Nobuo; Kawai, Kazuya; Tanaka, Nobuhiro; Ueda, Kinzo; Akasaka, Takashi; Hanaoka, Keiichi Igarashi; Uemura, Shiro; Oda, Hirotaka; Katahira, Yoshiaki; Kadota, Kazushige; Kyo, Eisho; Sato, Katsuhiko; Sato, Tadaya; Shite, Junya; Nakao, Koichi; Nishino, Masami; Hikichi, Yutaka; Honye, Junko; Matsubara, Tetsuo; Mizuno, Sumio; Muramatsu, Toshiya; Inohara, Taku; Kohsaka, Shun; Michishita, Ichiro; Yokoi, Hiroyoshi; Serruys, Patrick W; Ikari, Yuji; Nakamura, Masato

2018-04-01

While primary percutaneous coronary intervention (PCI) has significantly contributed to improve the mortality in patients with ST segment elevation myocardial infarction even in cardiogenic shock, primary PCI is a standard of care in most of Japanese institutions. Whereas there are high numbers of available facilities providing primary PCI in Japan, there are no clear guidelines focusing on procedural aspect of the standardized care. Whilst updated guidelines for the management of acute myocardial infarction were recently published by European Society of Cardiology, the following major changes are indicated; (1) radial access and drug-eluting stent over bare metal stent were recommended as Class I indication, and (2) complete revascularization before hospital discharge (either immediate or staged) is now considered as Class IIa recommendation. Although the primary PCI is consistently recommended in recent and previous guidelines, the device lag from Europe, the frequent usage of coronary imaging modalities in Japan, and the difference in available medical therapy or mechanical support may prevent direct application of European guidelines to Japanese population. The Task Force on Primary Percutaneous Coronary Intervention of the Japanese Association of Cardiovascular Intervention and Therapeutics (CVIT) has now proposed the expert consensus document for the management of acute myocardial infarction focusing on procedural aspect of primary PCI.

Paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of prostate-specific antigen during acute myocardial infarction.

PubMed

Patanè, Salvatore; Marte, Filippo

2010-02-04

Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. Paroxysmal atrial fibrillation is a frequent complication of acute myocardial infarction. It has been reported that subclinical hyperthyroidism is not associated with coronary heart disease or mortality from cardiovascular causes but it is sufficient to induce arrhythmias including an increase in atrial fibrillation rate. It has also been reported that increased factor X activity in patients with subclinical hyperthyroidism represents a potential hypercoagulable state. Moreover chronic renal failure presents an increased arrhythmic risk. Apparently spurious result has been reported in a work about mean serum prostate-specific antigen (PSA) concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of serum PSA concentration in a 90-year-old Italian man during acute myocardial infarction. Also this case focuses attention on the importance of a correct evaluation of subclinical hyperthyroidism and of chronic renal failure. Moreover, our report also confirms previous findings and extends the evaluation of PSA during acute myocardial infarction. Copyright 2008 Elsevier Ireland Ltd. All rights reserved.

Regulation of signal transducer and activator of transcription 3 and apoptotic pathways by betaine attenuates isoproterenol-induced acute myocardial injury in rats.

PubMed

Zheng, P; Liu, J; Mai, S; Yuan, Y; Wang, Y; Dai, G

2015-05-01

The present study was designed to investigate the cardioprotective effects of betaine on acute myocardial ischemia induced experimentally in rats focusing on regulation of signal transducer and activator of transcription 3 (STAT3) and apoptotic pathways as the potential mechanism underlying the drug effect. Male Sprague Dawley rats were treated with betaine (100, 200, and 400 mg/kg) orally for 40 days. Acute myocardial ischemic injury was induced in rats by subcutaneous injection of isoproterenol (85 mg/kg), for two consecutive days. Serum cardiac marker enzyme, histopathological variables and expression of protein levels were analyzed. Oral administration of betaine (200 and 400 mg/kg) significantly reduced the level of cardiac marker enzyme in the serum and prevented left ventricular remodeling. Western blot analysis showed that isoproterenol-induced phosphorylation of STAT3 was maintained or further enhanced by betaine treatment in myocardium. Furthermore, betaine (200 and 400 mg/kg) treatment increased the ventricular expression of Bcl-2 and reduced the level of Bax, therefore causing a significant increase in the ratio of Bcl-2/Bax. The protective role of betaine on myocardial damage was further confirmed by histopathological examination. In summary, our results showed that betaine pretreatment attenuated isoproterenol-induced acute myocardial ischemia via the regulation of STAT3 and apoptotic pathways. © The Author(s) 2014.

Effect of hydrogen sulfide on inflammatory cytokines in acute myocardial ischemia injury in rats

PubMed Central

LIU, FANG; LIU, GUANG-JIE; LIU, NA; ZHANG, GANG; ZHANG, JIAN-XIN; LI, LAN-FANG

2015-01-01

Hydrogen sulfide (H2S) is believed to be involved in numerous physiological and pathophysiological processes, and now it is recognized as the third endogenous signaling gasotransmitter, following nitric oxide and carbon monoxide; however, the effects of H2S on inflammatory factors in acute myocardial ischemia injury in rats have not been clarified. In the present study, sodium hydrosulfide (NaHS) was used as the H2S donor. Thirty-six male Sprague Dawley rats were randomly divided into five groups: Sham, ischemia, ischemia + low-dose (0.78 mg/kg) NaHS, ischemia + medium-dose (1.56 mg/kg) NaHS, ischemia + high-dose (3.12 mg/kg) NaHS and ischemia + propargylglycine (PPG) (30 mg/kg). The rats in each group were sacrificed 6 h after the surgery for sample collection. Compared with the ischemia group, the cardiac damage in the rats in the ischemia + NaHS groups was significantly reduced, particularly in the high-dose group; in the ischemia + PPG group, the myocardial injury was aggravated compared with that in the ischemia group. Compared with the ischemia group, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) in the serum of rats in the ischemia + medium- and high-dose NaHS groups were significantly reduced, and the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) protein in the myocardial tissues of rats was significantly reduced. In the ischemia + PPG group, the TNF-α, IL-1β and IL-6 levels in the serum were significantly increased, the expression of ICAM-1 mRNA was increased, although without a significant difference, and the expression of NF-κB was increased. The findings of the present study provide novel evidence for the dual effects of H2S on acute myocardial ischemia injury via the modulation of inflammatory factors. PMID:25667680

Coronary arterial BK channel dysfunction exacerbates ischemia/reperfusion-induced myocardial injury in diabetic mice.

PubMed

Lu, Tong; Jiang, Bin; Wang, Xiao-Li; Lee, Hon-Chi

2016-09-01

The large conductance Ca(2+)-activated K(+) (BK) channels, abundantly expressed in coronary artery smooth muscle cells (SMCs), play a pivotal role in regulating coronary circulation. A large body of evidence indicates that coronary arterial BK channel function is diminished in both type 1 and type 2 diabetes. However, the consequence of coronary BK channel dysfunction in diabetes is not clear. We hypothesized that impaired coronary BK channel function exacerbates myocardial ischemia/reperfusion (I/R) injury in streptozotocin-induced diabetic mice. Combining patch-clamp techniques and cellular biological approaches, we found that diabetes facilitated the colocalization of angiotensin II (Ang II) type 1 receptors and BK channel α-subunits (BK-α), but not BK channel β1-subunits (BK-β1), in the caveolae of coronary SMCs. This caveolar compartmentation in vascular SMCs not only enhanced Ang II-mediated inhibition of BK-α but also produced a physical disassociation between BK-α and BK-β1, leading to increased infarct size in diabetic hearts. Most importantly, genetic ablation of caveolae integrity or pharmacological activation of coronary BK channels protected the cardiac function of diabetic mice from experimental I/R injury in both in vivo and ex vivo preparations. Our results demonstrate a vascular ionic mechanism underlying the poor outcome of myocardial injury in diabetes. Hence, activation of coronary BK channels may serve as a therapeutic target for cardiovascular complications of diabetes.

Asymptomatic cardiovascular manifestations in diabetes mellitus: left ventricular diastolic dysfunction and silent myocardial ischemia.

PubMed

Seferović-Mitrović, Jelena P; Lalić, Nebojsa M; Vujisić-Tesić, Bosiljka; Lalić, Katarina; Jotić, Aleksandra; Ristić, Arsen D; Giga, Vojislav; Tesić, Milorad; Milić, Natasa; Lukić, Ljiljana; Milicić, Tanja; Singh, Sandra; Seferović, Petar M

2011-01-01

Several cardiovascular manifestations in patients with diabetes may be asymptomatic. Left ventricular diastolic dysfunction (LVDD) is considered to be the earliest metabolic myocardial lesion in these patients, and can be diagnosed with tissue Doppler echocardiography. Silent myocardial ischemia (SMI) is a characteristic and frequently described form of ischemic heart disease in patients with diabetes. Objective The aim of the study was to assess the prevalence of LVDD and SMI in patients with type 2 diabetes, as well as to compare demographic, clinical, and metabolic data among defined groups (patients with LVDD, patients with SMI and patients with type 2 diabetes, without LVDD and SMI). We investigated 104 type 2 diabetic patients (mean age 55.4 +/- 9.1 years, 64.4% males) with normal blood pressure, prehypertension and arterial hypertension stage I. Study design included basic laboratory assessment and cardiological workup (transthoracic echocardiography and tissue Doppler, as well as the exercise stress echocardiography). LVDD was diagnosed in twelve patients (11.5%), while SMI was revealed in six patients (5.8%). Less patients with LVDD were using metformin, in comparison to other two groups (chi2 =12.152; p=0.002). Values of HDL cholesterol (F=4.515; p=0.013) and apolipoprotein A1 (F=5.128; p= 0.008) were significantly higher in patients with LVDD. The study confirmed asymptomatic cardiovascular complications in 17.3% patients with type 2 diabetes.

Unmet goals in the treatment of Acute Myocardial Infarction: Review

PubMed Central

Farah, Alejandro; Barbagelata, Alejandro

2017-01-01

Reperfusion therapy decreases myocardium damage during an acute coronary event and consequently mortality. However, there are unmet needs in the treatment of acute myocardial infarction, consequently mortality and heart failure continue to occur in about 10% and 20% of cases, respectively. Different strategies could improve reperfusion. These strategies, like generation of warning sign recognition and being initially assisted and transferred by an emergency service, could reduce the time to reperfusion. If the first electrocardiogram is performed en route, it can be transmitted and interpreted in a timely manner by a specialist at the receiving center, bypassing community hospitals without percutaneous coronary intervention capabilities. To administer thrombolytic therapy during transport to the catheterization laboratory could reduce time to reperfusion in cases with expected prolonged transport time to a percutaneous coronary intervention center or to a center without primary percutaneous coronary intervention capabilities with additional expected delay, known as pharmaco-invasive strategy. Myocardial reperfusion is known to produce damage and cell death, which defines the reperfusion injury. Lack of resolution of ST segment is used as a marker of reperfusion failure. In patients without ST segment resolution, mortality triples. It is important to note that, until recently, reperfusion injury and no-reflow were interpreted as a single entity and we should differentiate them as different entities; whereas no-reflow is the failure to obtain tissue flow, reperfusion injury is actually the damage produced by achieving flow. Therefore, treatment of no-reflow is obtained by tissue flow, whereas in reperfusion injury the treatment objective is protection of susceptible myocardium from reperfusion injury. Numerous trials for the treatment of reperfusion injury have been unsuccessful. Newer hypotheses such as “ controlled reperfusion”, in which the interventional

Infection Rate and Acute Organ Dysfunction Risk as Explanations for Racial Differences in Severe Sepsis

PubMed Central

Mayr, Florian B.; Yende, Sachin; Linde-Zwirble, Walter T.; Peck-Palmer, Octavia M.; Barnato, Amber E.; Weissfeld, Lisa A.; Angus, Derek C.

2013-01-01

Context Severe sepsis, defined as infection complicated by acute organ dysfunction, occurs more frequently and leads to more deaths in black than in white individuals. The optimal approach to minimize these disparities is unclear. Objective To determine the extent to which higher severe sepsis rates in black than in white patients are due to higher infection rates or to a higher risk of acute organ dysfunction. Design, Setting, and Participants Analysis of infection-related hospitalizations from the 2005 hospital discharge data of 7 US states and infection-related emergency department visits from the 2003-2007 National Hospital Ambulatory Care Survey. Main Outcome Measure Age- and sex-standardized severe sepsis and infection hospitalization rates and the risk of acute organ dysfunction. Results Of 8 661 227 non–childbirth-related discharges, 2 261 857 were associated with an infection, and of these, 381 787 (16.8%) had severe sepsis. Black patients had a 67% higher age- and sex-standardized severe sepsis rate than did white patients (9.4; 95% confidence interval [CI], 9.3-9.5 vs 5.6; 95% CI, 5.6-5.6 per 1000 population; P<.001) and 80% higher standardized mortality (1.8, 95% CI, 1.8-1.9 vs 1.0, 95% CI, 1.0-1.1 per 1000 population; P<.001). The higher severe sepsis rate was explained by both a higher infection rate in black patients (47.3; 95% CI, 47.1-47.4 vs 34.0; 95% CI, 33.9-34.0 per 1000 population; incidence rate ratio, 1.39; P<.001) and a higher risk of developing acute organ dysfunction (age- and sex-adjusted odds ratio [OR],1.29; 95% CI, 1.27-1.30; P<.001). Differences in infection presented broadly across different sites and etiology of infection and for community- and hospital-acquired infections and occurred despite a lower likelihood of being admitted for infection from the emergency department (adjusted OR, 0.70; 95% CI, 0.64-0.76; P<.001). The higher risk of organ dysfunction persisted but was attenuated after adjusting for age, sex, comorbid

Heart-type fatty acid binding protein (H-FABP) as a biomarker for acute myocardial injury and long-term post-ischemic prognosis.

PubMed

Ye, Xiao-Dong; He, Yi; Wang, Sheng; Wong, Gordon T; Irwin, Michael G; Xia, Zhengyuan

2018-05-17

Acute myocardial infarction (AMI) is a life-threatening event. Even with timely treatment, acute ischemic myocardial injury and ensuing ischemia reperfusion injury (IRI) can still be difficult issues to tackle. Apart from radiological and other auxiliary examinations, laboratory tests of applicable cardiac biomarkers are also necessary for early diagnosis and close monitoring of this disorder. Heart-type fatty acid binding protein (H-FABP), which mainly exists inside cardiomyocytes, has recently emerged as a potentially promising biomarker for myocardial injury. In this review we discuss the sensitivity and specificity of H-FABP in the assessment of myocardial injury and IRI, especially in the early stage, and its long-term prognostic value in comparison with other commonly used cardiac biomarkers, including myoglobin (Mb), cardiac troponin I (cTnI), creatine kinase MB (CK-MB), C-reactive protein (CRP), glycogen phosphorylase isoenzyme BB (GPBB), and high-sensitivity cardiac troponin T (hs-cTnT). The potential and value of combined application of H-FABP with other biomarkers are also discussed. Finally, the prospect of H-FABP is summarized; several technical issues are discussed to facilitate wider application of H-FABP in clinical practice.

Feasibility of Extracorporeal Shock Wave Myocardial Revascularization Therapy for Post-Acute Myocardial Infarction Patients and Refractory Angina Pectoris Patients.

PubMed

Myojo, Masahiro; Ando, Jiro; Uehara, Masae; Daimon, Masao; Watanabe, Masafumi; Komuro, Issei

2017-04-06

Extracorporeal shockwave myocardial revascularization (ESMR) is one of the new treatment options for refractory angina pectoris (RAP), and some studies have indicated its effectiveness. A single-arm prospective trial to assess the feasibility of ESMR using Cardiospec for patients with post-acute myocardial infarction (AMI) and RAP was designed and performed. The patients were treated with 9 sessions of ESMR to the ischemic areas for 9 weeks. The feasibility measures included echocardiography; cardiac magnetic resonance imaging; troponin T, creatine kinase-MB (CK-MB), and brain natriuretic peptide testing; and a Seattle Angina Questionnaire (SAQ) survey. Three post-AMI patients and 3 RAP patients were enrolled. The post-AMI patients had already undergone revascularization with percutaneous coronary intervention (PCI) in the acute phase. In two patients, adverse events requiring admission occurred: one a lumbar disc hernia in a post-AMI patient and the other congestive heart failure resulting in death in an RAP patient. No apparent elevations in CK-MB and troponin T levels during the trial were observed. Echocardiography revealed no remarkable changes of ejection fraction; however, septal E/E' tended to decrease after treatments (11.6 ± 4.8 versus 9.2 ± 2.8, P = 0.08). Concerning the available SAQ scores for two RAP patients, one patient reported improvements in angina frequency and treatment satisfaction and the other reported improvements in physical limitations and angina stability. In this feasibility study, ESMR seems to be a safe treatment for both post-AMI patients and RAP patients. The efficacy of ESMR for post-AMI patients remains to be evaluated with additional studies.

Asian dust exposure triggers acute myocardial infarction.

PubMed

Kojima, Sunao; Michikawa, Takehiro; Ueda, Kayo; Sakamoto, Tetsuo; Matsui, Kunihiko; Kojima, Tomoko; Tsujita, Kenichi; Ogawa, Hisao; Nitta, Hiroshi; Takami, Akinori

2017-11-14

To elucidate whether Asian dust is associated with the incidence of acute myocardial infarction (AMI) and to clarify whether patients who are highly sensitive to Asian dust will develop AMI. Twenty-one participating institutions located throughout Kumamoto Prefecture and capable of performing coronary intervention were included in the study. Data for ground-level observations of Asian dust events were measured at the Kumamoto Local Meteorological Observatory. Data collected between 1 April 2010 and 31 March 2015 were analysed, and 3713 consecutive AMI patients were included. A time-stratified case-crossover design was applied to examine the association between Asian dust exposure and AMI. The occurrence of Asian dust events at 1 day before the onset of AMI was associated with the incidence of AMI [odds ratio (OR), 1.46; 95% confidence interval (CI), 1.09-1.95] and especially, non-ST-segment elevation myocardial infarction was significant (OR 2.03; 95% CI, 1.30-3.15). A significant association between AMI and Asian dust was observed in patients with age ≥75 years, male sex, hypertension, diabetes mellitus, never-smoking status, and chronic kidney disease (CKD). However, Asian dust events had a great impact on AMI onset in patients with CKD (P < 0.01). A scoring system accounting for several AMI risk factors was developed. The occurrence of Asian dust events was found to be significantly associated with AMI incidence among patients with a risk score of 5-6 (OR 2.45; 95% CI: 1.14-5.27). Asian dust events may lead to AMI and have a great impact on its onset in patients with CKD. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com.

Right Ventricular Dysfunction Impairs Effort Tolerance Independent of Left Ventricular Function Among Patients Undergoing Exercise Stress Myocardial Perfusion Imaging.

PubMed

Kim, Jiwon; Di Franco, Antonino; Seoane, Tania; Srinivasan, Aparna; Kampaktsis, Polydoros N; Geevarghese, Alexi; Goldburg, Samantha R; Khan, Saadat A; Szulc, Massimiliano; Ratcliffe, Mark B; Levine, Robert A; Morgan, Ashley E; Maddula, Pooja; Rozenstrauch, Meenakshi; Shah, Tara; Devereux, Richard B; Weinsaft, Jonathan W

2016-11-01

Right ventricular (RV) and left ventricular (LV) function are closely linked due to a variety of factors, including common coronary blood supply. Altered LV perfusion holds the potential to affect the RV, but links between LV ischemia and RV performance, and independent impact of RV dysfunction on effort tolerance, are unknown. The population comprised 2051 patients who underwent exercise stress myocardial perfusion imaging and echo (5.5±7.9 days), among whom 6% had echo-evidenced RV dysfunction. Global summed stress scores were ≈3-fold higher among patients with RV dysfunction, attributable to increments in inducible and fixed LV perfusion defects (all P≤0.001). Regional inferior and lateral wall ischemia was greater among patients with RV dysfunction (both P<0.01), without difference in corresponding anterior defects (P=0.13). In multivariable analysis, inducible inferior and lateral wall perfusion defects increased the likelihood of RV dysfunction (both P<0.05) independent of LV function, fixed perfusion defects, and pulmonary artery pressure. Patients with RV dysfunction demonstrated lesser effort tolerance whether measured by exercise duration (6.7±2.8 versus 7.9±2.9 minutes; P<0.001) or peak treadmill stage (2.6±0.9 versus 3.1±1.0; P<0.001), paralleling results among patients with LV dysfunction (7.0±2.9 versus 8.0±2.9; P<0.001|2.7±1.0 versus 3.1±1.0; P<0.001 respectively). Exercise time decreased stepwise in relation to both RV and LV dysfunction (P<0.001) and was associated with each parameter independent of age or medication regimen. Among patients with known or suspected coronary artery disease, regional LV ischemia involving the inferior and lateral walls confers increased likelihood of RV dysfunction. RV dysfunction impairs exercise tolerance independent of LV dysfunction. © 2016 American Heart Association, Inc.

Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms.

PubMed

Sui, Xizhong; Gao, Changqing

2014-01-01

Huperzine A (HupA), an alkaloid used in traditional Chinese medicine and isolated from Huperzia serrata, has been shown to possess diverse biological activities. The present study was undertaken to evaluate the cardioprotective potential of HupA in myocardial ischemic damage using a rat model of acute myocardial infarction. HupA significantly diminished the infarct size and inhibited the activities of myocardial enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT). A significantly reduced activity of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD), of the non-enzymatic scavenger enzyme, glutathione (GSH), as well as of glutathione peroxidase (GSH-PX) were found in the HupA-treated groups. Furthermore, decreased protein levels of caspase-3 and Bax, and increased levels of Bcl-2 were observed in the infarcted hearts of the rats treated with various concentrations of HupA. In addition, treatment with HupA markedly inhibited the expression of the nuclear factor-κB (NF-κB) subunit p65, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These findings suggest that the cardioprotective potential of HupA is associated with its antioxidant, anti-apoptotic and anti-inflammatory properties in acute myocardial infarction in rats.

Discrete microstructural cues for the attenuation of fibrosis following myocardial infarction.

PubMed

Pinney, James R; Du, Kim T; Ayala, Perla; Fang, Qizhi; Sievers, Richard E; Chew, Patrick; Delrosario, Lawrence; Lee, Randall J; Desai, Tejal A

2014-10-01

Chronic fibrosis caused by acute myocardial infarction (MI) leads to increased morbidity and mortality due to cardiac dysfunction. We have developed a therapeutic materials strategy that aims to mitigate myocardial fibrosis by utilizing injectable polymeric microstructures to mechanically alter the microenvironment. Polymeric microstructures were fabricated using photolithographic techniques and studied in a three-dimensional culture model of the fibrotic environment and by direct injection into the infarct zone of adult rats. Here, we show dose-dependent down-regulation of expression of genes associated with the mechanical fibrotic response in the presence of microstructures. Injection of this microstructured material into the infarct zone decreased levels of collagen and TGF-β, increased elastin deposition and vascularization in the infarcted region, and improved functional outcomes after six weeks. Our results demonstrate the efficacy of these discrete anti-fibrotic microstructures and suggest a potential therapeutic materials approach for combatting pathologic fibrosis. Copyright © 2014 Elsevier Ltd. All rights reserved.

Effect and Safety of Morphine Use in Acute Anterior ST-Segment Elevation Myocardial Infarction.

PubMed

Bonin, Mickael; Mewton, Nathan; Roubille, Francois; Morel, Olivier; Cayla, Guillaume; Angoulvant, Denis; Elbaz, Meyer; Claeys, Marc J; Garcia-Dorado, David; Giraud, Céline; Rioufol, Gilles; Jossan, Claire; Ovize, Michel; Guerin, Patrice

2018-02-10

Morphine is commonly used to treat chest pain during myocardial infarction, but its effect on cardiovascular outcome has never been directly evaluated. The aim of this study was to examine the effect and safety of morphine in patients with acute anterior ST-segment elevation myocardial infarction followed up for 1 year. We used the database of the CIRCUS (Does Cyclosporine Improve Outcome in ST Elevation Myocardial Infarction Patients) trial, which included 969 patients with anterior ST-segment elevation myocardial infarction, admitted for primary percutaneous coronary intervention. Two groups were defined according to use of morphine preceding coronary angiography. The composite primary outcome was the combined incidence of major adverse cardiovascular events, including cardiovascular death, heart failure, cardiogenic shock, myocardial infarction, unstable angina, and stroke during 1 year. A total of 554 (57.1%) patients received morphine at first medical contact. Both groups, with and without morphine treatment, were comparable with respect to demographic and periprocedural characteristics. There was no significant difference in major adverse cardiovascular events between patients who received morphine compared with those who did not (26.2% versus 22.0%, respectively; P =0.15). The all-cause mortality was 5.3% in the morphine group versus 5.8% in the no-morphine group ( P =0.89). There was no difference between groups in infarct size as assessed by the creatine kinase peak after primary percutaneous coronary intervention (4023±118 versus 3903±149 IU/L; P =0.52). In anterior ST-segment elevation myocardial infarction patients treated by primary percutaneous coronary intervention, morphine was used in half of patients during initial management and was not associated with a significant increase in major adverse cardiovascular events at 1 year. © 2018 The Authors and Hospices Civils de Lyon. Published on behalf of the American Heart Association, Inc., by Wiley.

Right Ventricular Myocardial Stiffness in Experimental Pulmonary Arterial Hypertension: Relative Contribution of Fibrosis and Myofibril Stiffness.

PubMed

Rain, Silvia; Andersen, Stine; Najafi, Aref; Gammelgaard Schultz, Jacob; da Silva Gonçalves Bós, Denielli; Handoko, M Louis; Bogaard, Harm-Jan; Vonk-Noordegraaf, Anton; Andersen, Asger; van der Velden, Jolanda; Ottenheijm, Coen A C; de Man, Frances S

2016-07-01

The purpose of this study was to determine the relative contribution of fibrosis-mediated and myofibril-mediated stiffness in rats with mild and severe right ventricular (RV) dysfunction. By performing pulmonary artery banding of different diameters for 7 weeks, mild RV dysfunction (Ø=0.6 mm) and severe RV dysfunction (Ø=0.5 mm) were induced in rats. The relative contribution of fibrosis- and myofibril-mediated RV stiffness was determined in RV trabecular strips. Total myocardial stiffness was increased in trabeculae from both mild and severe RV dysfunction in comparison to controls. In severe RV dysfunction, increased RV myocardial stiffness was explained by both increased fibrosis-mediated stiffness and increased myofibril-mediated stiffness, whereas in mild RV dysfunction, only myofibril-mediated stiffness was increased in comparison to control. Histological analyses revealed that RV fibrosis gradually increased with severity of RV dysfunction, whereas the ratio of collagen I/III expression was only elevated in severe RV dysfunction. Stiffness measurements in single membrane-permeabilized RV cardiomyocytes demonstrated a gradual increase in RV myofibril stiffness, which was partially restored by protein kinase A in both mild and severe RV dysfunction. Increased expression of compliant titin isoforms was observed only in mild RV dysfunction, whereas titin phosphorylation was reduced in both mild and severe RV dysfunction. RV myocardial stiffness is increased in rats with mild and severe RV dysfunction. In mild RV dysfunction, stiffness is mainly determined by increased myofibril stiffness. In severe RV dysfunction, both myofibril- and fibrosis-mediated stiffness contribute to increased RV myocardial stiffness. © 2016 The Authors.

Antiarrhythmic effect of uridine and uridine-5'-monophosphate in acute myocardial ischemia.

PubMed

Bul'on, V V; Krylova, I B; Selina, E N; Rodionova, O M; Evdokimova, N R; Sapronov, N S; Mironova, G D

2014-10-01

Experiments on rats with acute myocardial ischemia accompanied by early postocclusive arrhythmias have shown normalizing, energy-stabilizing, and antiarrhythmic effects of uridine and uridine-5'-monophosphate. The drugs decreased lactate and restored reserves of glycogen and creatine phosphate depleted by ischemia. Uridine and uridine-5'-monophosphate significantly decreased the severity of ventricular arrhythmias. Both drugs reduced the incidence and duration of fibrillation. Uridine -5'-monophosphate demonstrated most pronounced antifibrillatory effectiveness. We hypothesize that the antiarrhythmic effect of the drugs is determined by their capacity to activate energy metabolism.

Association Between ACE Gene Polymorphism and QT Dispersion in Patients with Acute Myocardial Infarction.

PubMed

Karahan, Zulkuf; Ugurlu, Murat; Ucaman, Berzal; Veysel Ulug, Ali; Kaya, Ilyas; Cevik, Kemal; Sahin Adiyaman, Mehmet; Oztürk, Onder; Iyem, Hikmet; Ozdemir, Ferit

2016-01-01

Angiotensin converting enzyme (ACE) gene polymorphism is associated with high renin-angiotensin system causing myocardial fibrosis and ventricular repolarization abnormality. Based on these findings, this study was designed to determine the association between ACE gene insertion/deletion (I/D) polymorphism and QT dispersion after acute myocardial infarction (MI). The study included 108 patients with acute MI. Blood samples were obtained from all the patients for genomic DNA analysis. ECGs were recorded at baseline and at the end of a 6-month follow up. The OT dispersion was manually calculated. The mean age of the patients was 57.5 ±9.9 years (ranging from 36 to 70). The patients with DD genotype showed longer QT dispersion than patients with II or DI genotype at the baseline, while at the end of the six-month follow up the patients with DI genotype showed longer QT dispersion than patients with DD or II genotypes. However, the magnitude of the QT dispersion prolongation was higher in patients carrying the ACE D allele than patients who were not carrying it, at baseline and at the end of six-month follow up (52.5 ±2.6 msn vs. 47.5±2.1 msn at baseline, 57±3.2 msn vs. 53±2.6 msn in months, P: 0.428 and P: 0.613, respectively). Carriers of the D allele of ACE gene I/D polymorphism may be associated with QT dispersion prolongation in patients with MI.An interaction of QT dispersion and ACE gene polymorphism may be associated with an elevation of serum type I-C terminal pro-collagen concentration, possibly leading to myocardial fibrosis, and increased action potential duration.

Primary percutaneous coronary intervention for acute ST elevation myocardial infarction: Outcomes and determinants of outcomes: A tertiary care center study from North India.

PubMed

Dubey, Gajendra; Verma, Sunil Kumar; Bahl, Vinay Kumar

Primary percutaneous coronary intervention (PCI) is the current standard of care for acute ST elevation myocardial infarction (STEMI). Most of the data on primary PCI in acute STEMI is from western countries. We studied the outcomes of primary PCI for acute STEMI at a tertiary care center in North India. Consecutive patients undergoing primary PCI for STEMI were prospectively studied during the period from February 2103 to May 2015. The outcomes assessed were all cause in hospital mortality, factors associated with mortality, major adverse cardiac and cerebrovascular event rate (composite of all cause in hospital mortality, non-fatal re infarction and stroke) and procedural complications. 371 patients underwent primary PCI during the study period. The mean age was 54 years and 82.7% were males. The mean total ischemia time and door to balloon times were 6.8h and 51min respectively. 96.4% patients underwent successful primary PCI. The total in hospital mortality was 12.9%. Mortality with cardiogenic shock at presentation was 66.7% while non-shock mortality was 2.6%. In hospital MACCE rate was 13.5%. Factors significantly associated with mortality were KILLIP class (OR: 8.4), door to balloon time (OR 1.02), final TIMI flow (OR 0.44) and severe LV dysfunction (OR 22.0). Procedure related adverse events were rare and there was no non-CABG associated major TIMI bleeding. Primary PCI for acute STEMI is feasible in our setup and associated with high success rate, low mortality in non-shock patients and low complication rates. Copyright © 2016. Published by Elsevier B.V.

Multiple organ dysfunction syndrome, an unusual complication of heroin intoxication: a case report and review of literature.

PubMed

Feng, Gang; Luo, Qiancheng; Guo, Enwei; Yao, Yulan; Yang, Feng; Zhang, Bingyu; Li, Longxuan

2015-01-01

Multiple organ dysfunction syndrome (MODS) has rarely been described in patients with heroin intoxication. Here, we report a rare case of MODS involving six organs, due to heroin intoxication. The patient was a 32-year-old Chinese man with severe heroin intoxication complicated by acute pulmonary edema and respiratory insufficiency, shock, myocardial damage and cardiac insufficiency, rhabdomyolysis and acute renal insufficiency, acute liver injury and hepatic insufficiency, toxic leukoencephalopathy, and hypoglycemia. He managed to survive and was discharged after 10 weeks of intensive care. The possible pathogenesis and therapeutic measures of MODS induced by heroin intoxication and some suggestions for preventing and treating severe complications of heroin intoxication, based on clinical evidence and the pertinent literature, are discussed in this report.

Acute hypopituitarism associated with periorbital swelling and cardiac dysfunction in a patient with pituitary tumor apoplexy: a case report.

PubMed

Ohara, Nobumasa; Yoneoka, Yuichiro; Seki, Yasuhiro; Akiyama, Katsuhiko; Arita, Masataka; Ohashi, Kazumasa; Suzuki, Kazuo; Takada, Toshinori

2017-08-24

Pituitary tumor apoplexy is a rare clinical syndrome caused by acute hemorrhage or infarction in a preexisting pituitary adenoma. It typically manifests as an acute episode of headache, visual disturbance, mental status changes, cranial nerve palsy, and endocrine pituitary dysfunction. However, not all patients present with classical symptoms, so it is pertinent to appreciate the clinical spectrum of pituitary tumor apoplexy presentation. We report an unusual case of a patient with pituitary tumor apoplexy who presented with periorbital edema associated with hypopituitarism. An 83-year-old Japanese man developed acute anterior hypopituitarism; he showed anorexia, fatigue, lethargy, severe bilateral periorbital edema, and mild cardiac dysfunction in the absence of headache, visual disturbance, altered mental status, and cranial nerve palsy. Magnetic resonance imaging showed a 2.5-cm pituitary tumor containing a mixed pattern of solid and liquid components indicating pituitary tumor apoplexy due to hemorrhage in a preexisting pituitary adenoma. Replacement therapy with oral hydrocortisone and levothyroxine relieved his symptoms of central adrenal insufficiency, central hypothyroidism, periorbital edema, and cardiac dysfunction. Common causes of periorbital edema include infections, inflammation, trauma, allergy, kidney or cardiac dysfunction, and endocrine disorders such as primary hypothyroidism. In the present case, the patient's acute central hypothyroidism was probably involved in the development of both periorbital edema and cardiac dysfunction. The present case highlights the need for physicians to consider periorbital edema as an unusual predominant manifestation of pituitary tumor apoplexy.

PINK1 alleviates myocardial hypoxia-reoxygenation injury by ameliorating mitochondrial dysfunction

DOE Office of Scientific and Technical Information (OSTI.GOV)

Li, Yang; Qiu, Liangxian; Liu, Xiping

PTEN inducible kinase-1 (PINK1) mutant induces mitochondrial dysfunction of cells, resulting in an inherited form of Parkinson's disease. However its exact role in the cardiomyocytes is unclear. The present study examined the function of PINK1 in hypoxia-reoxygenation (H/R) induced H9c2 cell damage and its potential mechanism. The H/R model in H9c2 cells was established by 6 h of hypoxia and 12 h of reoxygenation. The CCK8 and LDH assay indicated that the cell viability was obviously reduced after H/R. The expression of PINK1 was decreased in H/R-induced H9c2 cells compared with control group. The vector overexpressing PINK1 was constructed to transfect intomore » H/R-induced H9c2 cells. Our results showed that cell viability was increased, cell apoptosis and caspase 3, cytochrome C (Cyto C) levels were decreased after LV-PINK1 transfection. Furthermore, PINK1 overexpression stabilized electron transport chain (ETC) activity, increased ATP production, mPTP opening and mitochondrial membrane potential (MMP), inhibited ROS-generating mitochondria, implying PINK1 alleviates H/R induced mitochondrial dysfunction in cardiomyocytes. In addition, the TRAP-1 siRNA was transfected into PINK1 treated H9c2 cells after H/R to detected the molecular mechanism of PINK1 protecting cardiomyocytes. The results indicated that silence of TRAP-1 reversed the effects of PINK1 in H/R-induced H9c2 cells. In conclusion, these results suggest that PINK1 overexpression alleviates H/R-induced cell damage of H9c2 cells by phosphorylation of TRAP-1, and that is a valid approach for protection from myocardial I/R injury. - Highlights: • Effects of H/R on cell viability and PINK1 expression in H9c2 cells. • Effects of PINK1 on cell viability in H9c2 cells with H/R model. • Effects of PINK1 on mitochondrial dysfunction in H9c2 cells with H/R model. • PINK1 ameliorates H/R-induced H9c2 cells injury by activating p-TRAP-1.« less

A porcine model for acute ischaemic right ventricular dysfunction.

PubMed

Haraldsen, Pernille; Lindstedt, Sandra; Metzsch, Carsten; Algotsson, Lars; Ingemansson, Richard

2014-01-01

To establish an experimental model for acute ischaemic isolated right ventricular dysfunction and the subsequent haemodynamic changes. An open-chest porcine model with ischaemic dysfunction of the right ventricle induced by ligation of the three main branches supporting the right ventricular free wall. Invasive monitoring of mean arterial blood pressure (MAP), central venous pressure (CVP), left atrial pressure (LAP) and right ventricular pressure (RVP); ultrasonic measurement of cardiac output (CO) and calculation of haemodynamic parameters such as stroke volume (SV), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and right ventricular stroke work (RVSW) using standard formulae. The ischaemic challenge to the right ventricle resulted in a significant (≥30%) reduction in RVSW associated with an increase (6-25%) in CVP and reduction (8-18%) in pulmonary artery pressure (PAP) despite unchanged PVR, all reflecting the failing right ventricle. There was also a significant drop in CO (14-22%) despite unchanged LAP indicating lessened transpulmonary delivery of left ventricular preload due to the failing right ventricle causing the haemodynamic compromise rather than left ventricular failure. Supraventricular and ventricular arrhythmias occurred in three and two out of seven pigs, respectively-all of which except one were successfully resuscitated with cardioversion and/or defibrillation. This novel open-chest porcine model of induced ischaemia of the right ventricular free wall resulted in significant haemodynamic compromise confirmed using standard haemodynamic measurements making it useful for further research on acute, ischaemic isolated right ventricular failure.

Payments for acute myocardial infarction episodes-of-care initiated at hospitals with and without interventional capabilities.